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GESTIÓN DE RECURSOS COMPARTIDOS Descripción y objetivos

In document Documento de programación (página 28-31)

2  types   of  emboli  –   tiny   ones  that   produce   wedge  shaped  hemorrhagic   emboli  or   can   chip   off   large   ones.    Where   do   most   Pul   emboli   embolize  from?     MC  SITE   for   thrombosis  is  the  deep  veins  of  the  lower  leg.    This  is  NOT  the  most  common  site  for   embolization;   it   is   the   femoral   vein  (this   is   the   MC   site   for   embolization).     Makes   sense  b/c   venous   clots   propagate  toward  the  heart   (deep  veins  to  the  femoral  vein,   and  the  femoral  vein  is  a  larger  vessel,  therefore  it  is  more  likely  to  chip  off).    So,  the   femoral  vein  is  the  MC  site  for  embolization  to  the  lung.    The  deep  veins  are  the  MC   site   where   deep  venous   thrombosis   begins.     (when  it   get   to   the   femoral   vein,   it   is   dangerous   for   embolization).     So,   small  ones   produces   hemorrhagic   infarct   that   is   only  if  you  have  an  underlying  lung  dz.      If  I  have  a  small  embolus,  prob   won’t  infarct   b/c   don’t   have  abnormal  lungs.   However,   if   you  have   preexisting   lung   dz  you  will   infarct.     85%   of   the   time   embolus   will  not   produce   infarct.     However,  in  the  15%,   most   of   the  pts   with  infarcts   have   preexisting  lung   dz  (ie  they   are  smokers).     The   other  type  of  embolus  is   a  saddle  embolus  (it  is   huge)  and  blocks   off  the  ori5ices  of   the  pulmonary  vessels  and  pulmonary  arteries.    If  you  knock  off  at  least  3  out  of  the  5  

ori5ices,  you  are  dead  in  a  millisecond,  so   there  is  no  infarction  b/c   you  don’t   have   time  to  infarct.    It  produces  acute  right  heart  strain  and  immediate  death.    Screening   test  of  choice:  Ventilation  perfusion  scan  –  will  have   ventilation,  no  perfusion;  

conUirmatory  test  is  pulmonary  angiogram.

VII.  Restrictive  Pulmonary  Disease

Restrictive  –  something  is   restricting  it   from   5illing.    Example:  restricted  5illing  of   the  heart  =  restrictive  cardiomyopathy.    Or  restriction  in  5illing  up  of  the  lungs  with   air.     Have   2   terms:   compliance   (Uilling   term,   inspiration   term)   and   elasticity   (recoil,  expiration  term);  

For  restrictive  lung  dz,  picture  a  hot  rubber  bottle  for   restrictive  lung  dz.    The  hot   rubber   bottle   is   dif5icult   to   ‘blow  up’,  therefore   compliance   is  decreased  and  it   is   hard  to   5ill  the  lung  up  with  air.    So,  what’s   preventing  it  from  blowing  up?  Fibrosis   (interstial  5ibrosis,  MC’ly).    If  you  get  the  hot  water  rubber   bottle  5illed  with  air  and   let  the  air  out,  what  happens  to  the  elasticity?  Increases.    So,  compliance  is  decreased   and  cannot   5ill  it  up,  but  once  you  do  5ill  the  lung  up,  it  comes  out  quickly  (elasticity   increases).    

Example:  pt  with  sarcoid  –  diff  to  5ill  lungs,  but  get  it  out  fast  (due  to  5ibrosis).  So,  all   TLC,   RV,   TV   (all   lung   capacities   have   all   equally   decreased).     FEV1/FVC   on   spirometer  –  take  a  deep  breath  (ie  pt  with  sarcoid)  –  FEV1  (amount  you  get   out  in   one   sec   –   normally   it   is   4   liters)   is   decreased,   FVC   (total   that   got   out   after   deep   inspiration)  is   decreased  (b/c  increased  elasticity)  –  this   is  the  same  as  FEV1,  so   the   ratio  is  often  1.    Normally,  the  FVC  is  5  liters,  and  the  FEV1  is  normally  4  liters  –  so,   the  normal  FEV1/FVC  ratio  is  4/5  =80%.    B/c  the  elasticity  is   increased,  the  FVC  is   the  same  as  FEV1,  and  therefore  the  ratio  is  increased  to  1  instead  of  0.8.  

Examples  of  restrictive  lung  dz’s:

1.    Pneumoconiosis  –  airborne/dustborne  dz’s  –  famous  in  big  cities  (LA,  NY).    Cole   worker   pneumoconiosis   –   esp.   in  west   Virginia/Penn,   have   an   anthrocotic   pigment   that  causes  a  5ibrous  rxn  in  the  lung,  leading  to  restrictive  lung  dz.    Have  an  increased   incidence  of  TB,  but  not  cancer.

2.  Silicosis  –  Sandblasters  get  graf5iti  off  things,  or  work  in  foundries  and  deal  with   rocks   (ie  quartz),  and  break   them   down,  and  breathe   in  dust,   leading   to   silicoses).    

Have  nodules  in  the  lung  that  are  hard  has  rock  (literally)  b/c  there  is  quartz  in  them   and  it  looks  like  metastatic  dz  in  the  lung  (silica  dioxide  –  which  is  sand  in  the  lung)  –   again,  increased  of   TB,   not  cancer.    If  pt   happens   to   have  rheumatoid  arthritis,  and   also   has   one   of   these   pneumoconiosis   (ie   Cole   workers),   have   a   potential   for   a   syndrome,   which   is   called   caplan   syndrome.     Caplan   syndrome   consists   of   rheumatoid  nodules  in  the  lung  (same  as  extensor  surfaces  in  the  arm).    Rheumatoid   arthritis   commonly   involves   the   lung   with   5ibrosis.     And   rheumatoid   nodules   can   form   in  the  lung.    The   combo  of   rheumatoid  arthritis  (rheumatoid  nodules)  in  

the   lung,   plus   pneumoconiosis   (silicosis/asbestosis/Cole   workers)   =   caplan   syndrome.    

3.     Asbestos   –   asbestos   5ibers   look   like   dumbbells   (therefore   ez   to   recognize).    

These  are  called  ferruginous   bodies.    Asbestos  5ibers  coated  with  iron,  therefore  can   call  them   either  asbestos  bodies  or  ferruginous  bodies.    MC  pulmonary  lesion  assoc   with  asbestos  is  not   cancer  –  it  is  a  5ibrous  plaque  with  a  pleura,  which  is  b9  (not   a   precursor   for   mesothelioma).     MC   cancer   assoc   with   asbestos   =   primary   lung   cancer,  2nd   MCC  =  mesothelioma,   which  is  a  malignancy   of  the  serosal  lining  of   the  lungs.    If  you  are  a  smoker  and  have  asbestos  exposure,  you  have  an  increased   chance  of  getting  primary  lung  cancer.     This  is  a  good  example  of  synergism  (other   causes  of  lung  cancer  (SCC)  include  smoking,  alcohol).    Asbestos  +  smoker  =  will  get   cancer.     There   is   no   increased   incidence   of   mesothelioma   with   smoking   (not   synergistic).    Example:    Roofer  for  25  years,  nonsmoker  (do   tell  you,  but  you  had  to   know  that  25  years  ago,   all  the  roo5ing  material  had  asbestos  in  it;  in  other  parts  of   NY,  many  buildings  were  torn  down,  and  there  was   asbestos   in  the  roo5ing  of  those   buildings,  which  was  inhaled  by  many  people,  and  10-­‐30  years   later  they  developed   primary  lung   cancer   or  another   complication   of  asbestosis).    What   would  he  most   likely  get?   Primary  lung  cancer  (primary  pleural  plaque  was  not  there).    If  he  was   a   smoker?   Primary   lung   cancer.     Mesothelioma  takes   25-­‐30  years  to   develop.     Lung   cancers  take  about  10  years  to  develop.    Lung  cancers  are  more  common,  and  you  die   earlier.    What  is  the  main  cause  of  asbestos  exposure?  Roofers  or  people  working  in  a   naval   shipyard   (b/c   all   the   pipes   in   the  ship   are   insulated   with  asbestos),   also   in   brake  lining  of  cars  and  headgear.

4.    Sarcoidosis  =2nd  MCC  restrictive  lung  dz.    

Example:    classic   x-­‐ray  –   lymph  nodes   (hilar   lymph  nodes   are  big),  haziness   seen,   too,   which   is   interstial   5ibrosis.     Sarcoid   is   a   granulomatous   dz   that   has   NO   relationship  to   infection  (cause  =  unknown).    Causes  a  noncaseating  granuloma   (not  caseating  b/c   no   relationship  to  TB  and  systemic   fungal  infections).    The  lungs   are   ALWAYS   involved   (lungs   are   the   primary   target   organ),   and   more   common  in   blacks.    Example:    black  person,  35  y/o,  with  dyspnea,  see  hilar  nodes  on  x-­‐ray,  uviitis   (blurry   vision   –   this   is   in5lammation   of   the   uveal   tract   –   this   dz   always   affects   something  in  the  face,  and  the  face  the  2nd  MC  site  a  lesion  will  occur  with  this  dz,  can   also   involve   salivary   glands   or   lacrimal   glands   –   something   in  the  head/neck/face   area  (behind  the  lungs).    This  dz  is  a  dx  of  exclusion,  therefore  must  rule  out  anything   that   causes   granuloma  (TB,   Histo),   along   with  the   correct   physical  presentation   =   Sarcoidosis.    Rx  =  steroids.    ACE  enzymes  are  very  high  in  these  pts  b/c  granulomas   in   kidney;   hypercalcemia   –   macrophages   (epitheloid   cells)   make   1-­‐alpha-­‐

hydroxylase.     If   they   are   making   1-­‐alpha-­‐hydroxylase,   what   is   the   mech   of   hypercalcemia?   Hypervitaminosis   D.    you  are  second  hydroxylation  more  vit   D  and   therefore   have   excess   vit   D,   and   vit   D   promotes   reabsorption   of   calcium   and  

phosphorus,   leading   to   hypercalcemia.     This   is   the   MC   noninfectious   cause   of   granulomatous   hepatitis   (TB   is   the   MCC   of   infectious   hepatitis,   2nd   MC   =   pneumoconiosis).

5.    Hypersensitivity  pneumonitis  (farmer’s  lung,  siloUillers  dz,  bysinosis) These  are  restrictive  lung  dz’s.    Don’t   confuse  farmer’s  lung  and  silo5illers  dz  –  they   are  BOTH  seen  in  farmers.    So,  remember  one,  the  other  is  the  other!

SiloUillers  dz  –  put  things  in  silos,  which  is   a  closed  space,  and  fermentation  of  gas   occurs,  the  gas  is  nitrogen  dioxide  –  Example:    farmer  went   into   a  room  in  his  barn   and   suddenly   developed   wheezing   and   dyspnea,   why?   B/c   he   took   in   nitrogen   dioxide,   which   is   a   fermenting   problem.     (silo   can   explode   b/c   gas   from   fermentation).

Farmer’s  lung  –  thermophilic  actinomyces  (a  mold).    

Example:    on  tractor,  dust  being  blown  up  in  the  air  and  thermophilic  actinomyces   (which  is   a  mold)  is   inhaled;  leading  to   hypersensitivity   and  HPY  pneumonitis  and   they  end  up  with  a  restrictive  lung  dz.

Bysinosis  –  worker   in  textile   industry,  and  they   get   dyspnea.     These  are  the   HPY   and  restrictive  lung  dz’s.

Goodpasture  syndrome  

Begins   in   the   lungs   with   a   restrictive   lung   dz   (with   coughing   up   blood   –   hemoptysis),  and  ends   up  very  shortly  with  renal  dz  (therefore,  it  starts   in  the  lung   and  ends  in  the  kidneys).    This  is  a  restrictive  lung  dz.

VIII.  Obstructive  lung  Dz

In document Documento de programación (página 28-31)