Block B

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  1. What is rickets?
    It is a swelling of the costochondral junction.
  2. From what type of tissue are made the ribs? And if you find an extra rib?
    Normally they are made from bone and cartilage (except for #11-12 which are just bone). The extra rib would be made of dense connective tissue on C7 (cervical) or L1(lombar) vertebrae.
  3. What is the difference between separation and dislocation of the ribs?
    • Separation: separation at the costochondral junction
    • dislocation: separation at the sternocostal junction
  4. What are the 4 types of joints?
    • sychondrosis (primary) --> hyaline cartilage
    • Symphysis (secondary) --> fibrocartilage
    • Syndesmosis --> fibrous
    • Synovial *prone to osteoarthritis
  5. For each of these junctions, name the good type of joint: costochondral, sternocostal, manubriosternal, xiphisternal, costovertebral
    • -costochondral: primary
    • -sternocostal: 1st rib -->primary
    •                     other rib --> synovial
    • -manubriosternal: secondary
    • -xiphisternal:primary
    • -costovertebral: synovial
  6. What is the direction of external intercostal muscle? of internal intercostal muscle? of inner most intercostal muscle?
    • external --> downward medially
    • internal --> downward laterally
    • innermost --> upward laterally

    *thorasic transversus is part of the innermost layer
  7. Towards the 6th rib, the intercostal artery duplicates and bifurcate. Name the arteries, their direction and their role.
    • Musculophrenic artery: is going sideway to give blood supply to the diaphragm.
    • Superior epigastric artery: is going downward to give blood supply to the abdominal muscle.
  8. Name the structure that are in the hilum and their respective position.
    • arteries : superior anterior
    • veins : inferior anterior
    • bronchi : posterior
  9. What are the particularity of the left lung? Why is this clinically relevant?
    • There is only 2 lobes.
    • There is a cardiac notch(between rib 4 and 5) that permits the access to the heart without risking the perforation of the pleural space.
    • The lingula (under the notch) acts as a 3rd lobe.
  10. In a embryo, when will the respiratory system begin its formation?
    Around the 4th week, at the beginning of the embryonic phase.
  11. What occurs during the embryonic phase of the embryo development concerning the respiratory system? (4-7 week)
    • There will be the formation of the trachea-oesophagus septum.
    • The lung buds will fist into the pleural cavity made of mesothelium.

    * Don't forget that the tube is surrounded by mesenchyme.
  12. From which of the 3 layered embryo will the respiratory develop? Name the other layers as well
    • Endoderm
    • ectoderm
    • mesoderm
  13. Explain briefly the process between the endoderm and the formation of the trachea.
    The endoderm will form a tube called the primitive gut. This will become the digestion tube. A groove will develop from this tube and this will grow to form a second tube; the trachea!
  14. How is called the mutation that can cause a tracheo-oesophagus fistula(some parts stay connected)?
    SHH --> Sonic-hedge-hog
  15. What occurs during the pseudoglandular phase of the embryo development concerning the respiratory system?(7-16 week)
    The pseudocolumnar epithelial cells will communicate witht he mesenchyme, leading to an increased number of ducts
  16. What occurs during the canicular phase of the embryo development concerning the respiratory system?(16-26 weeks)
    There will be active angiogenesis at the growing tips.The bronchioles will branch into several alveolar ducts.
  17. What occurs during the Terminal sac phase of the embryo development concerning the respiratory system?(26-birth)
    The epithelium will differenciate into 2 types of cells, so there will be the apparition of surfactant.
  18. What occurs during the postnatal phase of the embryo development concerning the respiratory system?(birth-8 years)
    The alveoli will keep growing.
  19. What are the different phase of the embryonic development in regard of the respiratory system?
    • Embryonic (4-7 week)
    • pseudoglandular (7-16 week)
    • Canicular (16-26 week)
    • Terminal/saccular (26-40 week)
    • Alveolar/post-natal (birth-8 years)
  20. What produces the amniotic fluid?
    kidneys, lungs, skin, placental membrane and chord

    *if you have not enough : oligohydramnious
  21. What organs are responsible for amniotic fluid removal?
    GI tract, lungs, placental membranes and chord

    *if you have too much fluid : polyhydramnios
  22. What is the coelomic cavity?
    It is how the pleural space is called before the lung buds fist into it.
  23. What is the lymph node route for the lungs?
    bronchopulmonary, inferior tracheobronchial, superior tracheobronchiol, paratracheal.

    *left inferior lymph nodes will go to the RIGHT side
  24. What are the usual layers that are found in the conducting portion of the respiratory tract?
    • Mucosa : epithelium
    •              Lamina propria (including ducts)
    • submucosa : smooth muscle
    •                   denser (but still loose) connective tissue + glands
    •                   cartilage
    • adventitia : (dense connective tissue)
  25. Name all the structures neccessary to form a functional axoneme.
    • Basal body : Made of 9 triplets of microtubules
    • Cilia : Made of 9+2 doublet of microtubules interconected by nexin. There is also dynein (an ATPase) that promotes the mouvment of the cilia. From each microtubules at the surrounding, there is a radial spokes going toward the center.The 2 microtubules in the middle are surrounded by inner sheath.

    *Each microtubules are made of 13 protofilaments
  26. Name 2 mutations that can cause cilia immobility.
    • PCD : pulmonary cilia diskinesia
    • RSP : radial spoke protein 2
  27. What is particular in the olfactory epithelium?
    • There is microvili instead of cilia that beats
    • There is distal cilias that capt the odors
    • The neurons connect to the fila olfactoria nerve (not myelinated)
    • There are Bowman's gland in the lamina propria --> produce a serous fluid to wash out the cilia
  28. Why is the cartilage in a C-shape around the trachea?
    The other end of the C-shape (to close the ring) is smooth muscle. It permits some liberty to contract while swallowing.
  29. What characterize the respiratory epithelium?
    • pseudo stratified columnar ciliated epithelium
    • goblet cells (produce mucus)
    • short cells (not yet diffenrentiated)
    • brush cells (will become ciliated)
    • Granule cells (epinefrin + serotonin)
  30. Where is the only place where there are glands in the lamina propria?
    • In the nasal cavity : olfactory --> Bowmann's
    •                              non-olfactory --> normal glands
  31. Where, in the respiratory tarct, does the epithelium becomes folded?
    In the pulmonary bronchi
  32. Where, in the respiratory tract, can you see clara cells?
    In the small bronchioles(terminal + respiratory).

    *Clara cells are shorter and have no cilia, they produce surfactant.
  33. How is called the layer surroundig the cartilage?
  34. What does a small compliance mean?
    It means you have a stiff lung, because you need a big change in pressure to have a normal change in volume
  35. What is the formula to calculate the transpulmonary pressure?
    • Ptp=Pao-Ppl 
    • *ao--> airway opening
    • * when there is no flow Pao=Palv
  36. What is Laplace law?
    • It is an equation to calculate the difference of pressure between two luid (here surfactant and air)
    • P=2T/r (T--> tension)
  37. What is Reynold's number?
    • It evaluates the turbulence of a flow (bigger = more turbulent)
    • =2rvd/n (r-->radius, v-->velocity,d-->density, n-->viscosity)
  38. For a laminar flow, how can you find the resistance?
    • R=8nL/(πr4)
    • n-->density
    • L-->length
    • r-->radius
  39. What are the differences in laminar and turbulent flow?
    • Laminar : low flow rate
    •               small tube diameter
    •               middle is moving faster
    •               air is moving in a parallel fashion
    •               p is proportional to flow
    • Turbulent : high flow rate
    •                 big tube diameter
    •                 The mean velocity is the same everywhere
    •                 p is proportional to flow2
  40. What contribute to the smaller resistance in the smaller airways?
    • The total cross-sectional area increase(thus readucing the resistance)
    • The branching forms a parallele circuit (thus reducing the lenght of the tube)
  41. What are the accessory muscles in inspiration?
    • scalenes
    • trapezius
    • sternocleidomastoids
  42. What is the physiological dead space? the anatomical one? the alveolar one?
    • phyisiological is a sum of the other 2
    • anatomical is the normal dead space created by the airways that are only conducting the air (150 ml)
    • alveolar is when an alveolus gets air in, but there is no perfusion
  43. What are the 2 types of respiratory failure?
    • Type 1 : hypoxemia
    • Type 2: Hypercapnia
  44. Why is PVR (pulmonary vascular resistance) lower at higher flow?
    • vascular distension
    • vascular recruitment
  45. What are the 3 West's zones?
    • 1.PA > Pa > Pv
    • 2.Pa > PA > Pv
    • 3.Pa > Pv > PA

    *A --> alveolar, a-->arterial
  46. What is Henry's law?
    P=kc, at a constant T° the partial pressur is proportional to the concentration. k just being a different constant for each gas and liquid.
  47. How much oxygen can bind to hemoglobin?
    • 4 Molecules of O2 per hemoglobin
    • 1.39 ml of O2/g of Hb (normally between 12-15 g of hemoglobin in 100 ml of blood)
  48. What are the enzyme that facilitae the CO2 transport as bicarbonated ions?
    carbonic anhydrase
  49. How can you know PACO2 ?
    Image Upload
  50. How can you know PAO2 ?
    • Image Upload
    • R being = 85%
  51. What are the 5 causes of Hypoxemia?
    • Decreased PiO2
    • hypoventilation
    • V/Q mismatch
    • Shunt ( there is a normal shunt when the bronchial veins drain into the pulmonary veins)
    • Diffusion limitation
    • *dead space is not a hypoxemic cause (high V/Q)
  52. How can you know the affinity of a drug?
    Image Upload


    •         K1  
    • R + D ⇌ RD
    •          K2

    Low KD --> high affinity
  53. What does ADL's mean?
    Activities of daily life
  54. Knowing the KD, how can you caluclate the proportion of receptors occupied by a drug?
    Image Upload
  55. What is confounding by indication?
    It is when the prognostic factors influence the treatment only for a group of people. Eg : everyone with a more severe condition can be prescribed a different medication from people with only a mild type of this condition. This could lead to a bias in the results
  56. What is a sufficient causation?
    It is a combination of factor that will inevitably lead to disease
  57. What is a component causation?
    It is when a factor contributes to a disease, but will not inevitably lead to the disease
  58. What is a necessary causation?
    It is when a factor is needed for a diseas to occur
  59. Cigarette smoking increases the proteases causing emphysema, but it also has other effects on immune system. What are they?☺
    • increase # of neutrophils in lung tissue
    • delay neutrophil transit
    • increase neutrophil elastase synthesis and release
    • increase # of alveolar macrophage
  60. What are the 3 types of emphysema and their characteristics?
    • centrilobular : upper lobe more affected
    • panacinar : develops earlier than centrilobular, but less frequent
    •                 antiprotease deficiency (alpha-1-antitrypsin)
    •                 lower lob more affected
    • paraseptal : formation of bullae 
    •                   near the pleur in the upper lobe
  61. What are the different types of bronchiectasis?
    cylindrical, varicose, saccular
  62. What causes emphysema?
    • Too much proteinase/elastase
    • Not enough anti-proteinase
    • oxydative stress
  63. What can we do to treat COPD(normally include small airway disease + emphysema)?
    • smoking cessation/exercice
    • SABA/LABA (short/Long acting bronchodilators agents)
    • pulmonary rehabilitation
    • ICS (inhaled corticosteroids)
    • LTOT (long-term oxygen therapy)
    • surgery
  64. How many people in Canada suffer from asthma?
    8% of adult
  65. What are the steroid responsive factors involved during an inflammation?
    • Eosinophils, mast cells, CD4
    • IL-4, IL-5, IL-13 + IgE
  66. What are the steroid insensitive factors involved during an inflammation?
    • neutrophils, macrophages, CD8
    • TNF-alpha
  67. What are the physiological factors that can trigger asthma?
    stress, pregnancy, obesity, gastro-oesophageal reflux, sinus disease
  68. What is the threshold to determine if a bronchidilator is effective or not?
    You need to see an improvement of at least 12%, which acount for a change of at least 200 ml in FEV1 within 30 minutes
  69. How can you mesure if your airways are hyperresponsiveness?
    You give a bronchochonstrictor, like methalcoline or histamine. A normal person would keep approximatyvely the same FEV1. If you get a drop of 20% or more with less then 8mg/ml, then you have airway hyperresponsivness.
  70. What is considerated a well controlled asthma?
    • < 4 exacerbations during day/week
    • < 1 exacerbation during night/week
    • normal physical activity
    • no absenteism due to asthma
    • FEV1 > 85% of predicted
  71. What are the main differences between blue/green puffers and orange/red ones to treat asthma?
    • blue/green: bronchodilators, SABA, LABA, "-ol"  "-ium"
    • red/orange: ICS, "-one"  "-ide"
  72. How is ACTH produced?
    PVN (paraventricular nucleus) in the hypothalamus will send CRH(corticotropin releasing hormone) to the corticotrop cells (in anterior pituitary) that will activate and cleave POMC to produce ACTH.
  73. If you cleave ACTH, what do you get?
    you get alpha-MSH (melanocyte stimulating hormone) that can cause hyperpigmentation
  74. By what is regulated the HPA axis?
    stress and circadian regulation
  75. What part of the adrenal cortex does what hormone?
    • glomerulosa : aldosterone
    • fassiculata : glucocorticoids (GC)
    • reticularis : GC+ androgens
  76. How does the ACTH triggers the formation of the cortisol?
    The ACTH receptor is called MC2R and will, with the help of PKA and cAMP, phosphorylate StAR (steroidogenic acute regulatory protein) wich will increase the transport of cholesterol into the mitochondria. It will then be proced into pregnenolone, a pre-hormone.
  77. What are the functions of glucocorticoids?
    • increase blood glucose level
    • mobilize amino acids
    • stimulate lipolysis
    • catabolic effect on bone
    • inhibit immune function*
    • inhibit inflammation*

    *therapeutic functions
  78. What is Addison's disease?
    • auto-immune primary (at the adrenal level) insufficiency
    • muscular weakness, low blood pressure, weight loss, hyperpigmentation, hypoglycemia
  79. What is CAH (congenital adrenal hyperplasia)?
    • glucocorticoid insufficiency
    • increase adrenal androgen (b/c loss of negative feedback)
    • -shortened stature
    • -early puberty
    • -severe acne
    • -virilization + infertility in women
  80. What is Cushing's syndrome?
    • elevated cortisol
    • rapid weight gain
    • increased fat in face, trunk, base of neck
    • thinning + reddening of skin
    • thin arms and legs
  81. What are some side effect of GC?
    • GIO (GC induced osteoporosis)
    • Iatrogenic Cushing's syndrome
    • induction of diabetes
    • redistribution of fat
    • impaired wound healing
  82. What frequency should you use to have a view of deep structure in ultrasonography?

    And if you want a high resolution?
    • low frequency -> low resolution -> deep structure
    • high frequency -> high resolution -> structure at the surface
  83. What is part of the non-parenchymal interstitium?
    • inter-lobular septa
    • pleura
    • connective tissue around the larger vessels
  84. What is include in the "interstitium"?
    • basement membrane
    • collagen
    • elastic tissue
    • fibroblast
  85. What is sarcoidosis?
    • It is a multi-organ non-necrotizing
    • granulomas surrounded by lymphocytes.
    • hilar adenopathy (enlargement)
    • Is asymptomatic if you don't have fibrosis (1/3 of patients)
    • unknow etiology, but affected more young black women
    • Many patients don't really need a treatment, but steroids usually work (for a whil 50% will relapse)
  86. What is IPF(idiopathic pulmonary fibrosis)/UIP (usual interstitial pneumonia)?
    • It has a patchy distribution characterized by honeycombing
    • There is mature and active fibrosis.
    • Lead to a bad prgnostic (max 3 years), but steroids can improve
  87. What is NSIP (non-specific interstitial pneumonia)?
    • uniform ditribution
    • only mature fibrous tissue
  88. What is DAD (diffuse alveolar damage)/AIP (acute interstitial pneumonia)?
    • more or less diffuse distribution
    • hyaline membrane
    • protein-rich fluid also containing necrotized cell in the airspace
    • ARDS (acute respiratory distress syndrome)
  89. What is BOOP(bronchiolitis obliterans organizing pneumonia)/COP(cryptogenic organizing pneumonia)?
    • patchy distribution
    • fibrosis in respiratory alveolar, alveolar ducts, alveolar sacs
  90. What are the signs of restrictive/interstitial lung disease?
    • low compliance
    • high elastic recoil
    • low lung volume

    • usually non-productive cough
    • rapid and shallow respiration
    • clubbing, cyanosis
    • crepitations during auscultations
  91. What is a cholinergic junction and how does it work? Name the 2 types.
    • It is a junction where ACh is the transmitter. 
    • choline wil get inside the cell into a vesicule and will be converted to ACh. Then the vesicule will fuse with the presynaptic membrane releasing the ACh wich will activate pre and post synaptic receptors.
    • AChE (acetycholinesterase) will degrate the ACh into choline + acetate.
    • AChEI(AChE inhibitors) can cause poisoning b/c constant activation of post-synaptic receptors.
    • There are 2 kind of ACh receptor : mAChR (muscarinic) --> GPCR (g protein coupled receptor) and nAChR (nicotinic)--> LGIC (ligand gated ion channels)
  92. What is an adrenergic junction?
    It is a junction where  NE or E is the transmitter. Ther is the alpha and the beta receptors
  93. How is E(epinephrin) made?
    tyrosine ->DOPA ->DA (dopamine) -> NE(norepinephrine) -> E

    * this process is called catecholamine biosynthesis
  94. What are 2 enzymes important for catecholamine metabolism?
    • MAO (monoamine oxidase)
    • COMT (catecholamine-o-methyltransferase)
  95. What is the difference between a direct agonist and an indirect agonist concerning the sympathomimetic drug?
    • direct agonist : act on NE receptor
    • indirect agonsit : promote release of stored transmitter, inhibit reuptake, inhibit metabolism
  96. Where can we find mAChR? nAChR? and adrenergic receptor?
    • parasympathetic : mAChR -> smooth muscle, heart, some glands
    •                             nAChR -> skeletal muscle, CNS(ganglion)
    • sympathetic effect : adrenergic
  97. What are the 3 cancer that has the highest incidence among women? and mortality rate?
    • incidence : breast, lung, rectum
    • mortality : lung, breast, rectum
  98. What are the 3 cancer that has the highest incidence among men? and mortality rate?
    • incidence : prostate, lung, rectum
    • mortality : lung, rectum, prostate
  99. Name the 2 different stem cells
    • embryonic
    • adult stem cell (are more limitated for differenciation + low rate of replication)
  100. What are some example of oncogenes?
    • growth factors
    • growth factor receptors
    • signal transducing protein (RAS)
    • nuclear transcription factor (MYC)
    • cyclins and CDK (to promote replication)
  101. What is TP53 gene?
    • It is the regulator of the genome
    • it assists in DNA repair
    • cell apoptosis if needed
    • angiogenesis inhibitor
  102. What is the particularity of a neovasularization?
    • It is done by the same principle as metastases
    • the Endothelial cells have more fenestrations, are more permeable and have a faster cell division rate. They also secrete their own growth factor
  103. What does VEGF(vascular endothelial growth factor) do?
    • vasodilatation effect
    • stimulate angiogenesis
    • anti-immune effect
    • acts on surace endothelial cells
    • -it is upregulated by hypoxia, cytokines, hormones and other growth factor
    • - it is produced by inflammatory cells and various neoplasms
  104. What is the difference between a case-control study, a cohort study and a cross sectional study?
    • cross sectional : 4 groups (disease -> yes/no + exposure -> yes/no)
    • cohort study : 2 groups (exposure -> yes/no)
    • case-control : 2 groups (disease -> yes/no)
  105. How do you calculate rate ratio?
    incidence rate in exposed/incidence rate in unexposed
  106. How do you calculate odds ratio?
    • odds of exposure in case/odds of exposure in control.
    • *odds (if 2 yes and 8 no --> 2/8 (not 2/10))
  107. How do you calculate attributable risk?
    difference in incidence risk : exposed-unexposed
  108. How do you calcultae attributable ratio?
    incidence of exposed-incidence of unexposed / incidence in exposed
  109. How do you calculate a population attributable rate?
    rate of incidence in all - rate of incidence in unexposed
  110. How do you calculate a population attributable ratio?
    rate of incidence in all - rate of incidence in unexposed/ rate of incidence in all
  111. What is cor pulmonale?
    It is an hypertrophy of the right ventricle caused by a pulmonray hypertension. It will also create ankle edema or leg swelling
  112. Name some gene mutation that can occur in the cell proliferaton pathway that can cause cancer?
    • k-ras : associated with smoking
    •            worse relative prognostic(compared with other mutation)
    •            lack of benefit from TKI(tyrosine kinase inhibitor) therapy
    • EGFR : associated with non-smoker
    •            good predicted response for TKI
    • ALK : high response rate with iritoztinib

    • *receptor (EGFR) -> k-ras -> raf -> cell proliferation
    •              EML4-ALK↗                 ↘prevention of cell death
  113. What are the principle characteristics of squamous cell carcinoma?
    • proximal
    • intraluminal growth
    • central necrosis + cavitation
    • hypercalcemia (b/c of thyroid-like hormone)
    • keratinization + intracellular bridge
    • best relative prognostic
  114. What are the principle characteristics of small cell carcinoma?
    • proximal
    • neuroendocrine function (causing Cushing's disease)
    • compression of the airway
    • worse realtive prognostic
    • metastasis very easily
    • high N/C ratio (nucleus/cytoplasm)
    • almost only seen in smokers
  115. What are the principle characteristics of large cell carcinoma?
    • peripheral
    • well circumscribed
    • no evidence of differentiation
    • necrosis
  116. What are the principle characteristics of adenocarcinoma?
    • Peripheral
    • most frequent lung cancer
    • divided in 4 categories --> acinar, papillary, bronchioloalveolar and mixed(whcih is in situ + invasive)
    • old scar carcinoma
  117. What is SVCO syndrome?
    It occurs in patient with lung cancer and it is characterized by facial swelling and collateral veins
  118. What is Pancoast syndrome?
    It occurs in patient with lung cancer and it is characterized by pain in the arm or the hand.
  119. What is Horner's?
    It occurs in patient with lung cancer and it is characterized by ptosis (falling eye lid), myosis(constriction od the pupil) and anhydrosis(decreased sweating). It is caused by the compression of the sympathetic pathway.
  120. What are the possible stage for a small cell lung cancer (SCLC)?
    • limited --> fits within 1 radiaton field
    • extensive
  121. What are the treatments for a NSCLC?
    • surgery for early stage disease
    • chemo + radio for locally advanced
    • palliative therapy for metasasis disease

    * you need to base the choice of the chemo treatment on the hisology of the cancer
  122. What are the treatments for a SCLC?
    • chemo + radio for limites
    • chemo for extensive

    *you can expect improvement after 1st treatment, 90% will respond
  123. What is the MRC(medical research council) grading system?
    It is to evaluate the dyspnea of a person

    • 1 : Strenuous exercise
    • 2 : While going up a slight hill
    • 3 : Walks slower than contemporain
    • 4 : need a break after 100 m to catch up breath
    • 5 : can't leave the house or get dress
  124. What is the NYHA (New-York heart association) classification for?
    It evaluate the dyspnea in relation with a heart failure.
  125. What is the SVCS (superior vena cava syndrome)?
    When the vena cava is compressed, no blood can come back from the head to the heart. It causes swelling of the lips, of the tongue, headache
  126. What is bronchiectasis?
    It is an irreversible abnormal dilatation of the airways caused by inflammatory destruction of the walls (often associated with CF (cystic fibrosis)).

    • Airways are filled with purulent mucus
    • It can lead to colonization by bacteria and infections
  127. How can you diagnose bronchiectasis?
    • CT scan
    • sweat Cl- test (associated with cystic fibrosis)
    • sputum culture (most useful one)
  128. Cystic fibrosis is often associated with a abnormality in the fluid inside the airway. Explain how this abnormality can occur.
    • Autosomal recessive disease causes loss of CFTR (Cystic fibrosis transmembrane conductance regulator) gene.
    • this gene normally codes for chloride channel at the epithelial cell surface
    • if Cl- goes out of the cell -> water follows
    • So if you have a CFTR defect, no Cl- goes out, hence no water, hence a thicker mucus
    • This thicker mucus will cause more damage and so more fibrosis
  129. What are the signs for Cystic fibrosis?
    • pancreatic insufficiency : malabsorption of fat --> steatorrhea (fat feces) and Fat-soluble vitamins (ADEK) dificiency
    • Elevated sweat chloride level : CFTR gene mutation (>60 mEq/L)
    • persisted pulmonary infections : bacterial colonization, bronchiectasis, bronchitis
    • Meconium ileus : DIOS (distal ileal obstruction syndrome)
    • liver and biliary problems : biliary cirrhosis
    • infertility : 98% in male, 20% in female
    • *forme frustre -->mild or atypical symptoms (eg: chronis rhinosinusites)
  130. In pharmacokinectics, what does ADME stand for?
    • administration
    • distribution
    • metabolism
    • elimination
  131. What is the lipid solubility-cut off phenomenon?
    It is when a molecule, even if it is lipophilic, can't cross the cell membrane because of the presence of aqueous membrane.
  132. How does the pH influence the diffusion?
    • If you have a weak acid in a acidic/low pH (high H+), they will stay bounded to their H and thus stay uncharged.
    • If you have a weak basic in a basic/high pH (low H+), they will no try to bind to an extra H+, thus staying uncharged
    • All molecules can cross more easily if they are uncharged
  133. What is the first-pass effect?
    It is when a drug is absorbed in the gut and goes into the hepatic circulation before going into the systemic one. The molecule will most likely be metabolize at some degree by the liver
  134. What is the principles enzymes used in drug metabolism?
    50% of drug metabolism is done by CYP3A4/5 which is a subtype of liver P450 enzymes.
  135. What is the difference in clearance and durg clearance?
    • clearance : rate of drug elimination
    • drug clearance: rate of blood cleared from the drug
  136. What is the difference between first-order and zero-order elimination?
    • first order : predictable, depends on the concentration
    • zero order : unpredictable, independent of concentration
  137. What is DDT?
    It is an insecticide acting on the sodium channels in the nervous system. It causes uncotrolled repetitive spontaneous discharges along the nerves.
  138. What are the 2 types of adverse effects?
    • dose related : extension of the therpeutic effect
    • surprise toxicity : unrelated to the therapeutic effect
  139. Name the 4 virginia satir stances and what is considerated in each? (other/self/context)
    • placating : other + context
    • blaming : self + context
    • irrelevant : none
    • super-reasonable : context

    *the goal being to acheive congruence, a balance between other, self AND context
  140. What does URTIs stands for?
    upper respiratory tract infections
  141. What is pneumoconiosis?
    • It is a restrictive lung disease caused by different dust inhalation. 
    • It includes, asbestosis, silicosis, berylliosis
  142. What are the 2 types of asbestos?
    • serpentines : long curly strands -> chrysotile
    • amphibole : long straight
  143. What are the consequence of inhaling asbestos?
    • pleural plaques
    • asbestosis (inflammation + fibrosis of parenchymal)
    • lung cancer
  144. Associated the right column with the left one :
    a)Silicosis                                                 1)organic dust
    b)berylliosis                                             2)sand blasting
    c)hypersensitivity pneumonitis (HP)   3)granulomas disease(like sarcoidosis)
    • A-2
    • B-3
    • C-1
  145. Why does mycobacterium tuberculosis can survive in difficult condition, such as heat, light, dry air for a long period of time (can stay 24 hours in suspension in the air)?
    simply because it is protected by a thick waxy outer layer
  146. What are the principle events during the primary infection for TB?
    • slow moving and dividing bacteria, normally in the periphery of the lung. The primary lesion --> gohn focus(subpleural, at the apex)
    • spread to the lymph node
    • hemategenous dissemination
    • Cell mediated immunity finally kicks in, creating a granulomas response
  147. How can you diagnose a latent TB?
    • PPD : tuberculose skin test
    • IGRAS : interferon gamma release assays, trhough genomic, more specific
  148. How can you diagnose a active TB?
    • 3 sputum samples
    • microscopic exam (rapid but more or less sensitive)
    • cultures(high specificity and sensitivity, but long)
    • nucleic acid amplification (rapid + fairly sensitive)
  149. How can you treat active TB?
    • Multiple drug therapy
    • at least 6 months
  150. How can you treat latent TB?
    • only 10% will reactivate
    • single drug therapy
    • usually 9 months, compliance is hard, b/c they don't feel sick
  151. What does desmoplastic mean?
    proliferation of firboblast while the tissue is rejecting the tumor invasion
  152. What does atelectasis mean?
    No air
  153. What does myasthemia Gravis mean?
    It is a auto-immune problem with ACh receptors at neuromucular junction
  154. What is Ficks' law?
    • Image Upload
    • v : flow of gas diffusing through barrier
    • A : surface area
    • D : diffusion coefficient
    • P1-P2 : partial pressure difference
    • T : thickness of barrier
  155. What is the difference between diffusion and perfusion limitation?
    • diffusion limitation : Not enough time to equilibrate
    • perfusion limitation : It had time to equilibrate, so no more exchange occurs
  156. What is miliary tuberculosis?
    It is a lot of little white nodule that had spread into the lungs
  157. What are the 3 main types of pneumonias?
    • lobar : in lower lobe
    •            eg -> streptococcus
    • broncho : patchy appearance, centerd at small airways
    •                abscess formation and cavitation
    •                eg -> staphylococcus
    • interstitial : no significant exudate
    •                  mostly affect airway (but alos airspace in more advanced)
    •                  eg -> mycoplasma
  158. Name different type of pneumonia and an example of each.
    • typical : streptococcus pneumoniae
    • atypical : Mycoplasma pneumoniae
    • population selected : Staphylococcus aureus/ pseudomonas aeruginosa
    • virus : influenza
  159. What are some characteristics of streptococcus pneumoniae?
    • 90% are community acquired
    • rust coloured sputum, plueritic chest pain, acute onset
    • visible airbronchogram on CXR
  160. What are some characteristics of staphylococcus aureus?
    • mostly hospital acquired
    • post influenza
    • necrosis + cavitation
    • no air-bronchogram
  161. What are some characteristics of mycoplasma pneuoniae?
    • interstitial pneumoniae
    • most common atypical pneumonia
    • sore throat, myalgia, no fever, headace
    • Bullous myringitis (inflammation of the ear)
  162. What are some characteristics of pseudomonas aeruginosa?
    • micro-abscess with bacterial invasion, hemorrhage and necrosis
    • most are hospital acquired
    • purulent bleu/green sputum
  163. What are some characteristics of influenza?
    • seasonal
    • ARDS
    • risk of bacterial infection
  164. What are the 3 types of exudate?
    • uncomplicated : sterile, free flowing, normal pH
    • complicated : more or less sterile, more or less loculated, low pH
    • empyema : bacteria, loculated, low pH, pus
  165. What is the difference between hypoxia and hypoxemia?
    • hypoxia : low O2 delivery in the tissue
    • hypoxemia : low PO2 in the blood
  166. What are the 3 factors in the Virchow's triad?
    • endothelial injury : exposure of ECM, facilating platelet's action
    • hypercoagulability : can be genetic or acquired
    • abnormal blood flow : stasis allows platelets to contact endothelium
    •                                  prevent the inflow of clotting factor
  167. What are the lines of Zahn? and where can we see them?
    There are in a thrombus and each layer is made of either red cells or pale platelale and fibrin.
  168. What are the 4 possible outcomes for a thrombus?
    • propagation : occurs toward heart direction
    • embolizatin : breaks free from the wall
    • dissolution : fibrinolytic mechanisms
    • organization/recanalization : ingrowth of fibroblast, smooth muscls and endothelium cells/channels to let blood flow through thrombus
  169. Describe a pulmonary infarct.
    • It is a red infarct that usually occurs at the base near the pleural surface.
    • It has a wedge shpe, with the apex pointing toward the hilum
    • 10% are ischemic necrosis that will eventually lead to a scar
  170. What is a syncope?
    It is fainting because you don't have enough blood flow to the brain
  171. How can you diagnose a PE (pulmonary embolism)?
    • no specific test
    • compression ultrasonography : if venous defect (non compressibility)persists
    • CTPA : most common and reliable for the moment
  172. How do you manage PE?
    You give anticoagulation

    • unfractioned heparin : need to monitor, but easy to start and to stop
    • low molecular weight heparin : stable level with quick onset of action
    • Warfarin : takes 4-7 days for effect, need carefull monitoring, vitamin k antagonist
    • Newer agents: thrombin inhibitors and factor Xa inhibitors
    • *critical cases : thrombolysis or embolectomy
    • *treatment for at least 3-6 months
  173. Name the 3 types of trisomy we saw in class and an important characteristic to differentiate them.
    • Trisomy 21 : clinodactyly (curved 5th finger) + flat nasal bridge
    • Trisomy 13 (Patau) : polydactyly (extra finger)
    • Trisomy 18 (Edward) : rocker bottom feet, congenital diphragmatic hernia
  174. Describe the Birt-Hogg-Dubé syndrome.
    • cutaneous manifestations
    • history of pneumothorax
    • renal tumor
    • autosomal dominant disorder
  175. Describe the CCHS (congenital central hypoventilation syndrome)
    • hypoventilation
    • autonomic nervous system dysregulation
    • autosomal dominant disorder
  176. Describe the Pompe disease
    • glycogen strage disease/lysosomal storage disorder -> glycogen lake in muscle biopsy
    • cardiomegaly, hearing loss
    • Gowers sign -->difficulty to get up
    • autosomal recessif disorder leading to lack of enzymes
  177. What are the different type of cells in the carotid body?
    • type I : glomus cells (O2 sensing)
    • type II : sustentacular cells (support)
    • NF : fibres of carotic sinus nerve
  178. How does the cells in the carotid body send O2 changes to the brain?
    When it feels ↓ O2 -> closure of K+ channels -> cell depolarization ->opening of Ca+ channels ->release of transmitter->post-synaptic nerve
  179. Where are the CO2 sensors?
    On the ventrolateral surface of the medulla in the RTN (retrotrapezoid complex)
  180. What promotes wakefulness?
    • It is a reticular formation in the higher part of the brainstem(midbrain + hypothalamus)
    • The major neutransmitter are monoaminergic and oxinergic (OXR)
  181. What promotes sleep?
    The ventro-lateral pre-optic (VLPO) promotes sleep and GABA is the major neurostransmitter involved.
  182. What are some normal changes in respiratory control during sleep?
    • reduced drive output from the controller
    • reduced muscle activity
    • increase upper airway resistance
    • impaired compensation for added loads
    • reduced responses to ventilatory stimuli
    • reduced end-expiratory lung volume
  183. Describe OSA (obstructive sleep apnea).
    • characterised by repeated hypoxia-reoxygenation
    • Upper airway collapse (absence of airflow despite effort)
    • Can have cardiovascular complications
    • Need to give CPAP (continuous positive airway pressure)
  184. Describe CSA (central sleep apnea)
    • characterised by cheyne-stokes respiration
    • loss (or partial loss) of effort
    • treatment: IPAP (inspiratory positive airway pressure)
  185. In which phase of sleep is SAH (sleep associated hypoventilation) worse.
    During REM, O2 is even lower
Card Set:
Block B
2013-11-01 03:07:46

block B
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