Answers – Respiratory



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Answers – Respiratory





  1. Gas exchange, host defence, metabolism, repair, vocalisation

  2. Because gas exchange requires that it opens into outside environment

  3. Epithelial cells

  4. Bradykinin and prostaglandins

  5. Fibrosis

  6. Nostrils

  7. Oropharynx

  8. Soft palate

  9. Nasal cavities, nasopharynx, laryngopharynx and larynx

  10. Valve to prevent solids and liquids entering lungs

  11. Stratified squamous epithelium

  12. Columnar ciliated cells with interspersed goblet cells (respiratory epith)

  13. Internal maries

  14. 3 Scroll like bones

  15. lateral surface of the nasal cavity

  16. warmed and humidified

  17. nasal hairs

  18. resistance in nasal cavity is high, meaning respiratory muscles can’t get enough air in to meet increased demands for O2 in exercise

  19. auditory (Eustachian) tube

  20. paranasal air sinuses

  21. no-one really knows! ?crumple zone ?resonance for voice? Insulating dental roots?

  22. Medially and inferiorly

  23. Narrow slit, Sticks up above path of food, protected by folds

  24. Swallowing

  25. 8 – 10 cm

  26. bronchi, bronchioles, alveoli

  27. attachments to nearby muscles and bone

  28. cartilage rings

  29. becomes more irregular

  30. there isn’t any

  31. surfactant (phospholipid)

  32. star shaped

  33. C shaped

  34. 2nd rib – sternal angle

  35. R

  36. Lobar bronchi, segmental bronchi and bronchioles

  37. Right lung, lower lobe (R bronchus wider than left and more steeply down. Gravity)

  38. Inspiration

  39. Elastic recoil

  40. Bronchioles

  41. Phrenic

  42. C3 – 5

  43. Pleural cavities

  44. Mediastinum. Trachea, oesophagus, heart, great vessels, nerves and lymph vessels

  45. Capillary endothelium, fused basement membrane, alveolar epithelium

  46. Costal (convex), mediastinal and diaphragmatic

  47. Pleura

  48. 2 – visceral and parietal

  49. xiphoid anteriorly and T12 posteriorly

  50. costal margin

  51. intercostals muscles

  52. pulls them upwards, increasing the AP and transverse diameters

  53. 2 – 3 cm above the clavicle – stabbings in shoulder can still puncture lungs

  54. reduces pressure to lower than that of atmospheric air

  55. lowest region of pleural cavity – in expiration not occupied by lung because diaphragm pressed closely against lower part of the rib cage

  56. L = 2, R = 3

  57. Pulmonary circulation

  58. Synthesise and secrete mucus

  59. Mucins, proteoglycans, glycosaminoglycans

  60. Albumin, alpha-1-antitrypsin

  61. Combat microorganism and phagocyte proteases

  62. Combat oxidants inhaled and released from activated phagocytes

  63. Goblet cell hyperplasia – mucus hypersecretion and more viscous

  64. Mucus not cleared as no cilia working = infection = damage to cilia

  65. No

  66. Clear mucus and toxins it has trapped out of respiratory tract

  67. 80%

  68. metasynchronously. Smoking = asynchronous beating

  69. pushed towards epiglottis – swallowed or expectorated

  70. larger cf ciliated cells – project into lumen

  71. bronchi and bronchioles

  72. phase 1 and phase 2, anti-oxidants, anti-proteases, lysosyme

  73. cytochrome p450 oxidases

  74. metabolise foreign compounds, can convert precarcinogens to carcinogens

  75. metabolism of foreign compounds

  76. phase 2 enzyme

  77. aleveoli

  78. type 1

  79. type 1 = flat, type 2 = rounded or columnar

  80. proliferate and differentiate into type 1 cells

  81. surfactant

  82. prevent bronchioles and alveoli collapsing by reducing surface tension

  83. premature babies (Premature Infant Respiratory Distress Syndrome)

  84. emphysema

  85. fail to differentiate into type 1 cells

  86. gas exchange

  87. macrophages, neutrophils

  88. macrophages

  89. neutrophils and macrophages respectively

  90. neutrophils

  91. serine proteases, metalloproteinases

  92. neutrophil elastase

  93. oxidants

  94. alpha-1-antitrypsin, tissue inhibitor of MMP respectively

  95. contain phase 1 and 2 enzymes

  96. connective tissue synthesis (eg elastin, collagen, fibrin)

  97. interstitial pulmonary fibrosis = too much, emphysema = reduced

  98. secrete mediators that stimulate epithelial cell division

  99. barrier controlling leukocyte migration, gas exchange

  100. 15 – 20%

  101. chronic bronchitis, emphysema, small airways disease

  102. fused basement membrane, one cell thick, close to alveolar epith

  103. lungs, chest wall – rib cage, respiratory muscles, parts of CNS controlling respiration, conducting airways

  104. conducting zones = upper airways plus ~16 generations of bifurcation at top of lung, no gas exchange taking place respiratory zones = last 7 generations of bronchiolar branching = gas exchange

  105. areas of lung that act as the conducting zone – are ventilated, but no gas exchange takes place

  106. 150ml

  107. process by which inspired air reaches the alveoli. Diffusion = process by which gases cross the gas-blood interface

  108. spirometry

  109. respiratory rate x (tidal volume – deadspace). Amount of fresh inspired air available for gas exchange per minute

  110. pulmonary ventilation increases much more than alveolar ventilation – why?

  111. Both pulmonary and alveolar ventilation will increase significantly

  112. 5 l/min (= total CO)

  113. rate of production of CO2, rate of consumption of O2, alveolar ventilation

  114. partial pressure of gas in mixture independent of pressures of other gases in mixture. Hence, Pgas = %gas x Ptotal

  115. inspired air is warmed and humidified

  116. functional residual capacity = amount of air in lungs at end of quiet expiration = expiratory reserve volume + residual volume = ~ 3L

  117. 500ml

  118. volume of air possible to inhale at end of a quiet expiration = tidal volume + inspiratory reserve volume

  119. Can’t measure residual volume with spirometry as this air is always present in the lungs to prevent them collapsing

  120. TLC

  121. Maximum volume of air that can be exhaled from lungs following a maximal inspiration = IRV + TV + ERV

  122. Using a tracer gas eg helium in spirometer. Known conc and volume before, measure conc after inhalation and exhalation. Hence calculate RV

  123. At end of tidal volume

  124. Inspired air is warmed and humidified

  125. RV and FRC (because problems breathing out)

  126. Interstitial pulmonary fibrosis, paraquat poisoning

  127. Problems with breathing in not out – though in practice, usually a mixture

  128. IRV and therefore VC and TLC

  129. = obstructive, so increased RV and FRC. Reduced ERV and VC.

  130. ~13.3kPa

  131. ~5.3 kPa

  132. because it has a similar molecular weight but is much more soluble (Fick’s Law)

  133. concentration of O2 free in solution (ie not bound to a carrier)

  134. The amount of O2 able to be asorbed in plasma would be massively insufficient to meet the body’s demands. Cardiac output would have to be increased by ~ 16x to compensate for this

  135. 15 g/dl

  136. 20 ml/dl in blood, 0.3 ml/dl in plasma

  137. Takes time for O2 to combine with Hb

  138. Free, as bicarbonate ions, combined to amino acids in plasma proteins (carbamino compounds)

  139. O

  140. Changing the pCO2 moves the equilibrium and changes the pH of blood. < pH = respiratory acidosis, >pH = respiratory alkalinosis

  141. Gas to blood (down partial pressure – concentration – gradient)

  142. Approximately equal

  143. Yes

  144. PCO2 at 5.3 kPa

  145. Yes

  146. Inappropriately high level of ventilation for the pCO2 (ie blowing off too much CO2

  147. low

  148. no

  149. pCO2.

  150. alters affinity of Hb for O2

  151. Hb concentration

  152. Age, gender

  153. Rate of O consumption, rate of blood flow

  154. Increases it

  155. Very little. O2 is not very soluble so the overwhelming majority of O2 in blood is bound to Hb. If Hb is nearly fully saturated, this will not change as pAO2 increases.

  156. Normal

  157. Ventilation is normal so pCO2 = normal. Hb concentration and pO2 are independent of each other

  158. Yes, because the total content of O2 in blood is low due to low Hb concentration

  159. Normal, ie ~ 15 breaths per min

  160. True

  161. No – increasing pAO2 will increase paO2, but this will not contribute to increasing Hb saturation or total O2 content

  162. Acidosis (because of CO2 retention)

  163. Hypoventilation, VQ mis-matching

  164. High pCO2

  165. Ventilation rate and rate of production of CO2

  166. Because O2 is not very soluble, so the amount of unbound O2 contributes very little to the total O2 content.

  167. If paO2 is very low, it may be driving respiration. If paO2 is increased via inspired O2, this respiratory drive will be turned off. This leads to increased pCO2 and respiratory acidosis

  168. Bronchitis

  169. Breath-holding – how does this work?

  170. Warming and humidification

  171. Hyaline

  172. Goblet cells, stored in mucin granules which coalesce on release

  173. Glands

  174. Mucous cells – produce mucins, serous cells – produce thinner secretion which helps wash mucus into airway

  175. 9,2

  176. dynesin, nexin

  177. 200

  178. mitochondria

  179. straight stroke moves mucus, then recovery = bent

  180. sperm tails

  181. secretion of mucus, movement of mucus, physical barrier, regulatory and inflammatory mediators

  182. chemokines attract cells, cytokines tell them what to do

  183. airway calibre – contraction and relaxation

  184. COX-2, iNOS

  185. Proliferation (hyperplasia) and hypertrophy

  186. Inter-cellular adhesion molecule

  187. Systemic

  188. Pulmonary

  189. One of the highest to any tissue

  190. Aorta

  191. Right heart

  192. Pulmonary veins take oxygenated blood to the left heart

  193. Dispersal of inflammatory mediators, drugs, gas exchange, supplies airway tissue and lumen with inflamm cells and proteinaceous plasma

  194. Platelet activating factor

  195. Neutrophil elastase

  196. Dilate vasculature, constrict smooth muscle, stimulate mucus secretion

  197. Secrete inflammatory mediators causing acute change (e.g. airway smooth muscle constriction) and induce airway remodelling when present over long time periods

  198. All obstruction of the airways but Asthma = variable, COPD = fixed, CF = mixture

  199. Smooth muscle cell hypertrophy / hyperplasia, thickened basement membrane, interstitial fibrosis, goblet cell hyperplasia, submucosal gland hypertrophy, angiogenesis

  200. Wheezing, dyspnea, cough – symptoms reversible

  201. Mucus hypersecretion, airway constriction, dehydration causes increased viscosity of mucus

  202. Things in the blood-stream (eg. Inflammatory mediators)

  203. Mutations in Cystic Fibrosis Trans-Membrane Regulator gene which codes for a protein for a Cl- channel in membrane of secretory cells. Therefore increased sticky secretions

  204. 7q31

  205. ATP

  206. Usually affects people 45 – 75 yrs. Follows pattern of cigarette smoking. Highest in males but catching up in females. 3rd commonest cause of death in UK

  207. Activates onco-genes, damages genes ordering apoptosis eg bax, p53

  208. Dose-dependent relationship – concept of pack-years

  209. Give chemo – those cells responsive to it die out, those resistant survive and then proliferate

  210. 3/12 without treatment, 9/12 with

  211. 5.5% (under 6%)

  212. Small cell, Non-small-cell

  213. Non-small-cell = squamous cell, adenocarcinoma, large cell undifferentiated

  214. Haemoptysis, dyspnoea, hoarseness, finger clubbing, loss of weight, chest/shoulder pain

  215. Determines prognosis, efficacy of treatment types

  216. CXR, CT scan, bronchoscopy (including biopsy). Might do MRI scan of chest / brain (mets)

  217. Loss of angle of fingernail – angle >180 degrees

  218. If involvement of (L) recurrent laryngeal nerve, which runs close to lung

  219. Tumour secreting ACTH = corticotrophin

  220. Cushing’s Syndrome

  221. Prognosis and treatment efficacy (therefore, clinical decisions)

  222. Tumour, Nodal involvement, Metastases – staging system for lung ca

  223. 1 and 2, possibly 3 in some cases

  224. palliative – maybe some chemo, radiotherapy as palliative measure, symptom control

  225. Disease has usually developed significantly before diagnosis. Symptoms may be similar to those often experienced in smoking, delaying seeking of medical help. May be masked by eg bronchitis

  226. Squamous cell

  227. Red/orange/brown pigmented areas

  228. Tumours form glandular spaces

  229. Glistening = mucus

  230. Bifurcation of the trachea

  231. Involvement of lymph nodes on opposite lung. N = 4

  232. M0 = no distant metastases, M1 = mets (including same lung but different lobe)

  233. Stage 4, palliative

  234. Small cell

  235. Mets usually present by diagnosis, so always palliative

  236. Asbestos – prove industrial origin of disease

  237. Loss of cilia, stratified flat cells

  238. Yes

  239. Smoking

  240. Dysplasia – larger, stratified cells, thickening of epithelium

  241. When dysplastic cells fill whole epithelium above basement membrane

  242. Basement membrane not breached

  243. Squamous cell

  244. Virulent organism, compromised host defence

  245. Alveolar = pneumonia, airway = bronchitis

  246. Fever, shortness of breath, purulent sputum, cough, pleural pain, headache

  247. 24 hours

  248. white

  249. alveoli solid – filled with pus

  250. CHECK

  251. Bronchitis

  252. Destruction of cilia, Mucus hypersecretion, cough, purulent sputum,

  253. Recurrent infection, overwhelming infection in previously healthy person

  254. 5 – 10 %

  255. abnormal dilation of the airways

  256. infection

  257. bacterial infection – neutrophils = pus

  258. oral abx, nebulised abx, iv abx, physio, steroids

  259. congenital, post-infective, pneumonitis, mechanical, immunological

  260. aspiration of vomit (usually while drunk)

  261. CF

  262. Top

  263. Staph aurea

  264. Mechanical (mucocilliary escalator, epith barrier, surfactant) local (IgA, BALT, lysosyme, transferring, alveolar macrophages), systemic (neutrophils, complement)

  265. Hereditary = primary ciliary dyskinesia

  266. Acquired = viral infection, cigarette smoke

  267. Ultrastructural abnormalities in cilia causing them to be immotile or beat in slow disordered way

  268. Pneumonia in neonate, recurrent infections in childhood

  269. Autosomal recessive with incomplete penetrance

  270. Chest Infection via bronchiectasis, male infertility, middle ear disease, sinusitis

  271. Middle ear, nose, paranasal sinuses, auditory tube, bronchi, resp bronchioles, tail of spermatozoa

  272. Sinusitis, middle ear disease, male infertility, chest infection

  273. All organs round the wrong way

  274. Dextrocardia, bronchiectasis and chronic sinusitis

  275. Viral = watery, not easily cleared by cilia. Smokers = viscous

  276. Bacteria wins – death/serious disease. Host wins – recovery. Neither wins – chronic infection

  277. Infection – inflammatory mediators – remodelling of airway – infection

  278. ICAM (intercellular adhesion molecule), VCAM (vascular adhesion molecule) e-selectin

  279. Increased

  280. Endothelial

  281. Contain an ATPase – provides energy for cilia movement

  282. Metasynchronous

  283. + + Virulent / mechanisms for chronic infection

  284. toxin produced by strep pneum – punches holes in cells

  285. strep pneumonae

  286. LPS coat, -ve charge

  287. Proteases

  288. Degrade connective tissue

  289. Inflammation

  290. IL1-a and –b, TNF-a, IL 6, G-CSF

  291. IL8

  292. Don’t have cartilage to keep them open

  293. Eg neutrophil elastase

  294. Exoproducts impair host defence, enzymes, adherence, avoid immune surveillance

  295. Haemophilus influenzae

  296. Filtration of emboli, gas exchange, metabolism of vasoactive substances

  297. Ang1 to Ang2, serotonin, NA

  298. F – this is bronchial circulation, which is part of the systemic circ

  299. Whole CO each cycle with spare capacity for increased CO. In systemic circ, CO is divided between different tissues

  300. By having a high capacity and low resistance

  301. Syst circ has higher resistance

  302. Exercise, fever, tachycardia

  303. None

  304. L ventricle much thicker wall

  305. Pulmonary arteries have thinner walls with much less smooth muscle

  306. R = 25, 8, 15

  307. L = 120, 80, 100

  308. Pulmonary pulse pressures are much lower

  309. (pul arterial pressure – pul venous pressure)/CO = pressure gradient /flow

  310. PVR ~ 2 mmHg/L/min, SVR ~ 18 mmHg/L/min (much higher)

  311. Ductus areteriosus

  312. Fibrosis to form cord

  313. VIth branchcial arch

  314. In fetus, no gas exchange in lungs as they are not inflated. Pulmonary resistance is + + high but this is normal

  315. In fetus, both ventricles similar thickness

  316. After birth, remodelling over first few weeks leads to thinning of RV

  317. 60%

  318. Hydrostatic pressures increase with depth so greater in pulmonary capillaries at base of lung

  319. Zone 1 = apex, PA > Pa > Pv so capillaries mainly shut. Zone 2 = middle, Pa > PA > Pv some capillaries shut at venous end. Zone 3 = base, Pa > Pv > PA capillaries open

  320. Radioactive tracer gas inhalation

  321. Apices of lung

  322. Fever, exercise

  323. Recritument (increased number of vessels) and/or distention (increased size)

  324. Constriction of pulmonary circulation in areas of under-ventilation in response to low pAO2 to prevent blood going to those areas of lung

  325. Blood going to under-ventilated areas of lung

  326. Diverts blood from areas where gas exchange cannot take place because of consolidated alveoli

  327. When there is nowhere for the blood flow to be diverted to (ie recruitment and distention are not possible) ie when there is damage to the vascular bed

  328. Emphysema

  329. Complex signalling pathways – no-one really knows!

  330. R heart failure, peripheral oedema

  331. R heart failure, R ventricular hypertrophy

  332. VQ scans

  333. VQ mismatch

  334. Lung infarction

  335. Filtered

  336. Hydrostatic pressure (out), colloid osmotic pressure (in)

  337. Air pressure (out), surface tension (in)

  338. 0.5 ml/min

  339. Drains into lymphatic system

  340. Increased hydrostatic pressure, reduced colloid osmotic pressure, increased capillary permeability

  341. L heart failure, mitral stenosis. Starvation, endothelial damage

  342. Pulmonary oedema

  343. Terrified patient, breathlessness, frothy pink sputum, crackles, reduced compliance

  344. Blood passes from pulmonary circulation (R heart) to systemic (L heart) without oxygenation

  345. Anatomic – pulmonary arteriovenous malformations, physiological – insufficient hypoxic vasoconstriction so blood goes to areas of underventilation

  346. Reduced gas exchange, reduced filtering of small emboli, reduced metabolism vasoactive substances

  347. Lung elastic recoil and chest wall elastic recoil

  348. Functional Residual Capacity = RV + ERV

  349. Phospholipid and lipoprotein rich liquid. Type 2 alveolar cells

  350. Covers surface of alveoli reducing surface tension

  351. Emphysema

  352. Inspiration

  353. Augments it

  354. Exercise, obstructive lung disease

  355. Measure of stiffness of lung (amount of volume change produced per unit pressure change)

  356. Slope of pressure/volume curve

  357. (Alveolar pressure – airway pressure) / flow

  358. Pulmonary circulation

  359. Obstructive = increased exp resistance, restrictive = increased insp resistance

  360. TLC

  361. Increased in obstructive (hyperinflation), reduced in restrictive

  362. FEV1/VC

  363. >75% = restrictive, <75% = obstructive

  364. In restrictive disease,FEV1 may be bit reduced, but VC is significantly reduced = high ratio. In obstructive disease, FEV1 lowered but VC normal or high = long expiration time preferred = low ratio

  365. R

  366. Inhale, blow out as hard as can and keep blowing out for 6s

  367. Constriction

  368. Dilation

  369. Catecholamines, beta2 agonists

  370. .cigarette smoke, allergens

  371. Obstructive

  372. Physical barrier, absorbtion, secretion, macromolecular transport, maintaining balance between antigen responsiveness and tolerance

  373. MALT, GALT, BALT (in animals)

  374. Barriers and mediators

  375. Mucus, cilia, skin, and complement, lysosyme, transferring

  376. Antibodies and T cells

  377. When presented by a cell (MHC1 – CD8+ T cells, MHC2 – CD4+ cells)

  378. Viral, mycobacterial infection

  379. Helminth infection

  380. Sarcoidosis

  381. Imbalance of immune response skewing it to Th2 side

  382. 2 – Tc1 and Tc2

  383. IFN-gamma – viral infection, IL-4 and 5 – allergy at mucosal surfaces

  384. Th3 = CD4+CD25+CTLA-4+

  385. Industrialisation/cleaner conditions = less immune challenge early in life (esp. by viruses and bacteria) = less production IL10 = imbalanced immune response

  386. IL10

  387. Increased

  388. Eosinophils, mast cells

  389. Histamine, heparin, leukotrienes

  390. Basic proteins

  391. Smooth muscle hypertrophy and proliferation, mucus gland hypertrophy, goblet cell hyperplasis, angiogenesis, fibroblast proliferation, fibrosis, increased connective tissue deposition

  392. Wheeze, cough, dyspnoea, reversible

  393. Inherited Increased propensity to produce IgE

  394. IL3, 4, 5, 13, G-CSF, TNFalpha

  395. Inflammation, (tissue injury and repair)remodelling, endothelial and epithelial cell damage

  396. Histamine, PGD2

  397. Oedema

  398. Bradykinin

  399. Mucus secretion

  400. Basic eosinophil proteins, TNFalpha

  401. Establishment of normal flora, timing and dose of antigens

  402. tolerance

  403. glucocorticoids, receptor antagonists (histamine antagonists, leukotriene antagonists)

  404. Beta2 agonists

  405. Ipratropium

  406. Broncho-constriction, mucus hypersecretion and increased viscosity due to dehydration – mucus plugs

  407. Linear (in physiological region)

  408. S shaped

  409. paCO2

  410. 4.7 kPa – 6.3kPa

  411. Lowers height of dissociation curve but same shape. No change to saturation curve

  412. Shifts it to right

  413. Reduces Hb affinity for O2

  414. Fever

  415. Increased paO2

  416. 3

  417. Hypoxaemic (1), ventilatory (2), combined (3)

  418. VQ mismatch. Some areas normally ventilated, others under ventilated. Rise (small) in paCO2 and fall in paO2. Stimulates respiratory drive. Normally ventilated areas receive most of additional ventilation as other areas involved in disease. Increasing ventilation can reduce paCO2 but because of plateau of O2 saturation curve, cannot increase paO2 with any significance. Increased ventilation will not allow blood from well ventilated areas to compensate for that from under ventilated areas on mixing to normalise paO2

  419. Normal or low paCO2, Low paO2

  420. Asthma, bronchitis with obstruction, pneumonia, pulmonary oedema, pulmonary fibrosis

  421. Narrower range for paCO2 – 5.3 – 6kPa cf 5.3 – 13 kPa for paO2

  422. Type 2

  423. Disease of respiratory muscles, head injury, polio

  424. High paCO2, low paO2

  425. Patients with chronic hypoxaemic (Type 1) respiratory failure

  426. Cor pulmonale – R heart failure and peripheral oedema

  427. Cardiac output, Hb conc, O2 saturation, arterial-venous difference

  428. Reduced cardiac output, reduced Hb conc, reduced O2 saturation

  429. Fluid recusitation (inc venous return), inotropes, chronotropes, blood (in severe anaemia – but don’t need to get normal values), inspired O2

  430. Type 1 (hypoxaemic), Type 2 (ventilatory), Type 3 (combined)

  431. Treat underlying cause, O2, positive pressure ventilation, reduced VQ mismatching eg. inhaled vasodilators

  432. Inadequate oxygenation, inadequate CO2 clearance, inadequate maintenance of airway, electively

  433. CPAP, PS

  434. CPAP = continuous positive airway pressure (means end expiration pressure positive – PEEP). PS – pressure support – during inspiration

  435. Reduce effort needed during inspiration (leave balloon partly inflated)

  436. Can cause volutrauma/progressive lung injury. Can increase dead-space ventilation.

  437. Invasive positive pressure ventilation, non-invasive PPV

  438. Adult Respiratory Distress Syndrome

  439. ??! no-on really knows! Can be direct, indirect, trauma, sepsis

  440. High permeability pulmonary oedema, Loss of HPV – V/Q mismatch – atelectasis, volutrauma. Mix of diseased and normal lung. Breathlessness, refractory hypoxaemia

  441. Increased permeability of post-capillary venules allows leak of + + fluid in the interstitium. This pushes structures apart ie. increased distance to diffuse across

  442. Reduced paO2 while increasing O2 – implies not just diffusion/vent problem

  443. Where blood passes through pulmonary capillaries without oxygenation (ie is shunted from right to left heart without gas exchange)

  444. V/Q mismatch

  445. Volutrauma (high pressures/volumes in alveoli), atelectasis

  446. Bilateral diffuse infiltrate

  447. Microvascular shunt, deadspace ventilation respectively

  448. Reduce effort of breathing, help with drugs and physio to shift secretions

  449. Treat underlying cause, low pressure ‘protective’ positive pressure ventilation, reduce VQ mismatch via inhaled vasodilators eg prostacyclin, NO and prone positioning

  450. NO, prostacyclin

  451. This way, only reach and act on areas of lung normally ventilated, therefore selectively increase perfusion to those areas.

  452. Preserved lung usually top (deadspace), dependent lung usually bottom (shunt)

  453. Gravity – blood and interstitial fluid to bottom of lung

  454. Endothelium/epithelium activated, release of inflammatory mediators, mediators travel via bloodstream to distant sites, endo/epithelium activated

  455. Sepsis, SIRS

  456. Systemic Inflammatory Response Syndrom

  457. Regulate gas exchange, behavioural acts, maintain airways and lung function

  458. Maintain upper airway patency

  459. Those that are involved in respiration – diaphragm, intercostals, upper abdominals

  460. Inspiration and expiration

  461. miturition

  462. Glossopharyngeal, vagus, spinal accessory, hypoglossal

  463. Phrenic (diaphragm), spinal nerves (T1 – T12 and T12 – L1)

  464. Cervical plexus – C3 – 5

  465. Medulla – pre-Bot-C region

  466. Early inspiratory, late inspiratory, expiratory

  467. Medulla

  468. Interconnections to form a ‘pacemaker’

  469. Distinctive patterns

  470. Generate respiratory rhythm in isolation in absence of input

  471. Carotid bodies, aortic arch

  472. pCO2, pO2, pH

  473. central chemoreceptors in medulla

  474. not sensitive to hypoxia or pH

  475. body very sensitive to it so increases ventilation

  476. paO2 must reduce quite significantly before ventilation will increase

  477. normal respiration driven by CO2 not O2 (hypercapnic not hypoxic)

  478. lungs, larynx, pharynx

  479. spinal nerves

  480. trigeminal = nose, glossopharyngeal = pharynx

  481. breathlessness

  482. depends on the level. If above C4 not usually survivable (why?)

  483. supra-brainstem activity (over-riding it)

  484. cortex

  485. front top (in homunculus, near trunk region)

  486. primary motor cortex, primary sensory cortex, cerebellum, basal ganglia, supplementary motor area

  487. cortico-spinal tracts to – resp muscles, to brainstem

  488. loss of voluntary movement

  489. pons

  490. automatic via brainstem, voluntary via cortex, emotional via limbic

  491. voluntary and emotional

  492. gas exchange, behavioural functions, non-respiratory functions

  493. voluntary and emotional

  494. looking at breathing on purely chemical level

  495. changes – REM sleep, similar to awake, non-REM, bigger amplitude, slower

  496. REM – active brain but muscle atonia

  497. Relax

  498. Becomes less sensitive

  499. Reduces

  500. Reduces

  501. O2 dissociation curve shape –reduce pO2 quite a lot before sat drops

  502. Small reduction in pO2 = big drop in saturation

  503. Start off with reduced pO2 so on the steep part of O2 dissociation curve

  504. Nocturnal ventilatory failure

  505. I

  506. Because respiratory centres less sensitive to CO2 – needs to go up to ensure capnic drive continues

  507. Less

  508. Central chemoreceptors

  509. Can’t move – no voluntary control of muscles

  510. Collapses – tongue falls back over airway. Constrictor muscles relax

  511. More effort needed to maintain same amount of ventilation

  512. Subject with tracheostomy – pCO2 still rises

  513. Turbulent flow of air over vocal cords

  514. Point below which level of pCO2 is too low to trigger breathing

  515. In sleep apnoeic threshold goes up.

  516. Central = no drive to breathe because of lack of sensitivity of resp centres. Obstructive = respiratory effort, normal control pCO2 but not enough respiration as blocked upper airway

  517. E

  518. Congenital hypoventilation syndrome, heart failure

  519. Irritation of J-receptors due to pulmonary oedema/hypertension = hypoventilation.

  520. Surge of SNS activity – can have damaging effect on heart

  521. Dilator muscles dilate/stiffen pharynx. Gravitational forces and adipose tissue act inwards

  522. Lost tone of dilator muscles

  523. Daytime sleepiness, hypertension, exacerbation of diseases, risk of cerebral infarction, headache on waking

  524. Polycythaemia, R heart failure

  525. CPAP

  526. Inspiration

  527. Diaphragm – increases vertical volume, intercostals lift ribs, increasing ap and transverse diameter. Increased volume = reduced intrathoracic pressure

  528. Sternocleidomastoid, scalene

  529. Rotating and flexing head, bending neck

  530. None!

  531. Elastic recoil – of lungs and of abdominal organs

  532. Rectus abdominis, internal intercostals, internal and external obliques

  533. In exercise, obstructive lung disease – extra effort/larger volume air

  534. Rectus abdominis – leaning back

  535. Coughing, sneezing, speaking, vomiting, laughter

  536. Symptom = sensation prompting seeking of medical help, sign = something apparent on physical examination

  537. Cough, dyspnea, chest pain, wheeze

  538. Hyperinflated chest, cyanosis, crackles on auscultation, dullness to percussion

  539. 10 – 38%

  540. 3rd most common reason for GP consultation

  541. Up to 27% of general population

  542. Chest

  543. Rapidly adapting irritant receptors

  544. Mechanical, chemical irritants, inflammatory mediators

  545. Superior laryngeal nerve, vagus

  546. Medulla

  547. Large airways

  548. Muco-ciliary escalator

  549. Mucuc, oedema

  550. Rapidly adapting (A-delta) and slowly adapting

  551. Naso-pharynx, posterior wall of trachea, bronchi, larynx - epithelium

  552. Airways smooth muscle

  553. Yes

  554. Mechanical stimulus – eg inflation of lung

  555. Small myelinated nerve fibres

  556. Mechanical and chemical irritant stimulus, inflammatory mediators

  557. ‘free’ nerve endings

  558. Larynx, trachea, bronchi, lungs

  559. Chemical irritant stimuli, inflammatory mediators

  560. Neuropeptide inflammatory mediators

  561. Area near tractus solitarius nucleus

  562. There isn’t one – they’re independent

  563. Inspiratory, glottal closure, expiratory

  564. Airflow in in inspi. No airflow during glottal closure. Sub glottal pressure rises to peak when massive rise in air flow and explosive fast airflow with dropping sub-glottal pressure (expiratory phase)

  565. 5-hydroxytryptamine, gamma-aminobutyric acid (GABA)

  566. Asthma, eosinophilic bronchitis, pulmonary fibrosis, rhino-sinusitis, lung cancer, COPD

  567. Prevent complications

  568. Pneumothorax with sub cut emphysema, cough syncope, arrhythmias, intercostal muscle pain, headache, rupture of rectus abdominis, urinary incontinence

  569. Increased cough reflex

  570. Irritation in throat, chest, coughing paroxysms

  571. Cigarette smoke, perfume, laughing, deep breath,. Vigorous exercise, cold air, change in temp, crumble

  572. Narcotics – codeine, morphine. Non-narcotics

  573. Constipation, physical dependence

  574. Inhaled beta agonists, inhaled steroids

  575. Gastro-oesophageal reflux

  576. ACE inhibitors

  577. Anti-cholinergic

  578. Bronchitis

  579. Trigeminal = nose, glossopharyngeal and vagus = pharynx, spinal nerves = chest wall

  580. Lungs, larynx, phalynx

  581. Muscle damage, broken rib

  582. Herpes zoster

  583. Pleuritic, cardiac, referred, visceral (poorly localised, deep seated)

  584. Referred

  585. Gastro-intestinal (peptic ulcer), cardiovascular (MI, pericarditis) musculoskeletal (broken rib)

  586. Secondary somatic cortex

  587. Primary somatic cortex

  588. Touch = Aalpha, Abeta Pain = Adelta

  589. Dorsal horn

  590. Caudal medulla

  591. Visceral pain more poorly localised, deep-seated, harder to treat

  592. Visceral and chronic

  593. Shortness of breath

  594. Life-threatening

  595. From lungs/chest wall, chemoreceptors, exercising muscles, cognition, emotion etc

  596. Limbic, primary and secondary somato-sensory cotex

  597. Impaired pulmonary function (asthma, COPD, fibrosis, phrenic nerve paralysis), impaired CVS function, altered central ventilatory drive

  598. Myocardial disease, valve disease, pericardial disease

  599. Metabolic disease, metabolic acidosis, anaemia

  600. Treat underlying cause (treating dyspnea very difficult)

  601. Lung reduction surgery, drugs affecting brain eg, narcotics

  602. Improving general health, fitness, psychological well-being

  603. Embryonic, pseudoglandular, canalicular, saccular

  604. Embryonic – 0 – 6 weeks

  605. Laryngotracheal groove

  606. Ventral wall of pharynx

  607. Grown into pleural passages and formed lobes

  608. Tracheobronchial tree

  609. The tree resembles an exocrine gland

  610. 16 – 28

  611. Approximate to potential air space

  612. Respiratory bronchioles with attached alveoli

  613. Alveolar cells into type 1 and 2 pneumocytes

  614. Lung liquid

  615. Saccular

  616. Alveoli

  617. 21 x

  618. surfactant

  619. Cannalicular – approx 22 weeks

  620. Scaffold around which lung is developed

  621. FRC

  622. Absorbed

  623. Prevent baby drowning

  624. Hormonal response leads to stimulation of Beta receptor, shutting Cl- channel. Na+ channel into lung stimulated. Na brings H2O with it. Na out via Na/K pump

  625. T4, cortisol, adrenaline

  626. Inflammation, corticosteroids

  627. Increased surfactant production, absorbtion of lung liquid, lung more structurally sound – can cause problems in later life

  628. Hypoplasia eg if half of diaphragm is missing allowing abdominal contents to squash lung.

  629. Reduced lung liquid

  630. Mechanically unstable – prone to collapse, opens into outside environment – infection/irritation

  631. P = 2T/R

  632. Smaller alveoli should collapse, as air travels to bigger ones to equalise pressures

  633. Surfactant lowers surface tension so far that Laplace’s Law is trivial

  634. Phospholipids, neutral lipids, apoproteins

  635. Type 2 pneumocytes

  636. DPPC – 2,3-dipalmitoyl phosphatidylcholine

  637. A and D

  638. D

  639. Correct insertion of DPPC into phospholipid bilayer and other ordering of molecules

  640. Caesarian

  641. B

  642. Smoking

  643. Give artificial surfactant

  644. Surfactant deficiency – decreased FRC and inc deadspace – alveolar collapse – reduced compliance – inc work of breathing – epithelial damage – serum protein inhibition – hypoxia – respiratory acidosis – depleted surfactant

  645. Hyaline membrane disease

  646. Much less volume increase for increase in pressure. Inc pressures lead to epithelial damage

  647. Amniotic fluid, vernix

  648. Foramen ovale, ductus arteriosus

  649. Absorbed

  650. Increases

  651. Increased pulmonary blood flow, expansion of collapsed lung



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