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How Helicobacter Pylori can cause gastric ulcerations and how this can lead to cancers of the stomach INCLUDING NOTE PAGE - Piril Erel
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How Helicobacter Pylori can cause gastric ulcerations and how this can lead to cancers of the stomach INCLUDING NOTE PAGE - Piril Erel

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I have also uploaded a PDF version containing the notes on each slide in which, I discuss each slide carefully and accurately as possible. If you would like to view just the powerpoint please look at …

I have also uploaded a PDF version containing the notes on each slide in which, I discuss each slide carefully and accurately as possible. If you would like to view just the powerpoint please look at my other uploads.

I hope you enjoy my powerpoint presentation.
Thank you, Piril


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  • 1. Welcome  to  my  presenta/on,  Here  I  will  be  discussing  how  helicobacter  pylori  causes  gastric  ulcera/ons  and  how   this  can  be  linked  to  cancers  of  the  stomach.  I  hope  you  enjoy  the  following  slides       1  
  • 2. It  affects  around  50%  of  the  world’s  popula/on.  It’s  one  of  the  most  common  infec/ons  in  the  U.K.     Unless  it  is  treated,  the  infec/on  will  stay  for  the  rest  of  an  individuals  life.  Now  this  is  due  to  the  fact  that  H.pylori   will  not  show  any  symptoms  or  problems  caused  by  H.pylori  and  so  will  not  even  know  that  they  are  affected.   However,  further  complica/ons  may  indicate  the  presents  of  H.pylori  in  the  gut  and  will  then  allow  individuals  to   seek  medical  help.       Helicobacter  Pylori  is  a  gram-­‐nega/ve  spiral  shaped  bacterium  that  grows  in  mucus  layer  that  coats  the  inside  of   the  human  stomach.     Gram-­‐nega/ve  refers  to  the  thin  layer  of  pep/doglycan  and  presents  of  a  outer  membrane  in  the  helicobacter  cell   wall       Helicobacter  was  detected  by  Robin  Warren  who  was  a  pathologist  and  a  physician  named  Barry  Marshall  in   Australia.  Although  many  individuals  did  not  believe  Warren  &  Marshall  as  H.pylori  did  not  show  symptoms.  Barry   Marshall  had  decided  to  do  something  dras/c  and  drank  a  solu/on  of  H.pylori  and  within  2  weeks  developed  acute   symptoms  which  we  will  discuss  later  on     2  
  • 3. The  prevalence  of  H.Pylori  infected  varies  widely  by  geographic  area  it  can  be  seen  that  countries  such  as  South   America    and  Africa  have  the  highest  prevalence.  This  is  due  to  the  transmission  of  H.pylori.  It  is  mostly  transmiSed   through  contamina/on  of  water  and  food  which  is  much  more  likely  to  occur  in  3rd  world  countries  and  when  we   compare  these  percentages  with  those  such  as  The  united  states  or  united  kingdom  or  even  Australia,  we  can  see   here  that  the  sani/za/on  are  much  beSer  and  therefore  the  prevalence  is  much  more  lower.       Next  Slide   3  
  • 4. There  are  4  different  steps  that  helicobacter  pylori  does  in  order  to  affect  the  human  host.     1.  Firstly  there  is  the  addi/on  of  Helicobacter  Pylori  to  the  host  cell   2.  Secondly,  and  most  importantly  helicobacter  pylori  minimizes  the  content  of  the  acid  in  the  stomach     3.  it  colonizes     4.  and  finally  the  degrades  the  epithelial  cells     1à  The  addi/on  of  helicobacter  pylori  is  enabled  by  the  flagella  which  allows  the  bacterium  to  be  mo/le  and  also  permits  the   bacteria  to  propel  itself  through  the  gastric  fluid,  mucus  layer  and  finally  adheres  itself  to  the  epithelial  lipopolysaccharides  and   membrane  proteins,  using  this  it  interacts  with  epithelial  cells  of  stomach       2à  The  hydrochloric  acid  keeps  the  pH  of  the  stomach  strongly  acidic,  between  a  pH  of  one  and  two,  H.pylori  is  able  to  survive  in   acidic  condi/ons  but  as  the  stomach  pH  is  a  liSle  too  acidic  for  the  bacteria  it  uses  an  enzyme  to  raise  the  pH  around  the  bacteria  to   a  more  survivable  level.  Urease  enzyme  is  used  where  it  will  breakdown  urea  and  water  to  produce  carbon  dioxide  and  ammonia.   As  we  know  that  ammonia  is  a  base  and  HCl  is  an  acid  this  allows  a  neutralizing  reac/on  making  the  pH  of  the  stomach  increase.     3àThis  creates  a  microenvironment  for  the  bacterium  to  survive  this  allows  the  coloniza/on  of  more  and  more  H.Pylori  to  thrive  in   this  environment       4  
  • 5. Now  the  degrada/on  of  the  epithelial  cells  occurs  in  many  different  ways:   The  Vac  A  exotoxin  causes  injury  to  the  mucosal  membrane  by  inducing  altera/ons  in  mitochondrial  membrane   permeability  and  apoptosis,  it  also  s/mulates  pro-­‐inflammatory  signaling  and  increases  the  permeability  of  the   plasma  membrane.     Type  IV  secre/on  system  uses  a  pillus  to  inject  effectors  such  as  Cytotoxin-­‐associated  gene  A  -­‐  cagA  is  a  needle-­‐like   appendage  that  injects  a  toxin  which  remodels  ac/n  the  cytoskeleton  of  the  cell  thereby  disrup/ng  the  epithelial   barrier  and  facilita/ng  the  passage  of  Vac  A,  it  is  also  found  to  inhibit  apoptosis.     These  responses  altogether  inhibits  immune  response  by  T  cell  ac/va/on  and  prolifera/on  so  the  body  cannot   produce  an  immune  response  against  Helicobacter  pylori  and  this  is  the  development  of  gastric  ulcera/ons     Next  Slide   5  
  • 6. So  this  image  shows  the  propor/ons  of  individuals  with  differing  disease  severity  The  50%  of  the  worlds  popula/on   who  has  helicobacter  pylori  is  more  suscep/ble  in  developing  duodenal  ulcers  about  90%  compared  to  the   unaffected  popula/on.  The  development  of  gastri/s  is  more  likely  when  affected  with  the  bacterium.  There  is  a   nine  fold  risk  of  developing  precancerous  gastric  condi/ons  when  compared  with  individuals  with  and  without  the   bacterium.  Also  almost  all  cases  of  gastric  lymphoma  is  linked  to  helicobacter  pylori  being  present  in  the  human   host.  As  discussed  before  the  prevalence  of  helicobacter  pylori  in  individuals  and  country  is  strongly  associated   with  poor  socioeconomic  condi/ons.     Next  slide   6  
  • 7. How  helicobacter  pylori  leads  to  gastric  cancer  is  not  well  understood  but  some  ideas  are  put  forward  by  scien/st,   it  is  unclear  whether  it  is  one  specific  cause  or  a  collec/on  of  all  of  these  effects  of  helicobacter  pylori  which   increases  the  chance  of  gastric  cancer.  Long-­‐term  exposure  to  cagA  toxin  causes  chronic  inflamma/on  and  can   induce  oncogenesis,  this  inflamma/on  leads  to  a  damaged  mucosal  membrane  and  can  increase  the  carcinogenic   effect  of  risk  factors  leading  to  gastric  cancer  such  as  high  salt  intake  and  smoking.  Recent  research  suggest  that   cagA  may  lead  to  inac/va/on  and  altera/on  of  tumor  suppressor  proteins  such  as  p53  which  normally  leads  to   apoptosis  and  therefore  inac/va/on  can  promote  the  development  and  progression  of  gastric  cancer     Next  Slide   7  
  • 8. 80%  of  individuals  who  suffer  with  helicobacter  pylori  will  experience  chronic  gastri/s  which  is  characterized  by   chronic  inflamma/on  of  the  stomach  mucosa  which  is  caused  by  injury  to  the  gastric  mucosa  resul/ng  from  reflux   of  bile  and  pancrea/c  secre/ons  into  the  stomach  acer  adhesion  of  helicobacter  pylori.15-­‐20%  of  theses   individuals  will  further  develop  chronic  atrophic  gastri/s  known  as  Type  A  or  B  gastri/s  is  a  process  of  chronic   inflamma/on  of  the  stomach  mucosa  leading  to  loss  of  gastric  glandular  cells  and  their  eventual  replacement  by   intes/nal  and  fibrous  /ssues.  A  duodenal  ulcer  can  also  develop  due  to  the  corrosive  HCl  in  the  stomach  causing   inflamma/on  and  ulcers  to  area  of  epithelial  cells  that  are  infected  with  helicobacter  pylori.  Furthermore  1%  of   these  individuals  can  finally  be  presented  with  gastric  carcinoma       Next  Slide   8  
  • 9. Indiges/on  is  the  main  symptom  of  helicobacter  pylori  due  to  a  induced  ulcer  however  this  symptom  is  common   among  many  types  of  disorders,  so  can  be  difficult  to  link  to  helicobacter  induced  disorder.  Indiges/on  can  further   be  accompanied  by  dull  and  burning  pain  which  is  worse  on  an  empty  stomach  and  can  be  relieved  by  antacids   very  briefly.  This  burning  pain  can  last  for  minutes  to  hours  and  comes  and  goes  over  days  an  weeks.  Gastric   carcinoma  can  present  itself  as  weight  loss,  vomi/ng,  dysphagia  and  anemia.     Next  Slide     9  
  • 10. Blood  tests  are  used  to  measure  an/bodies  to  Helicobacter  pylori.  An/bodies  are  proteins  made  by  the  body’s  immune   system  when  it  detects  harmful  substances  such  as  bacteria.  Blood  tests  for  Helicobacter  pylori  can  only  tell  if  your  body  has   Helicobacter  pylori  an/bodies.  It  cannot  however  tell  if  you  have  a  current  infec/on  or  how  long  you  have  had  it,  this  is   because  the  test  can  be  posi/ve  for  years  even  if  the  infec/on  is  cured.  As  a  result  blood  tests  cannot  be  used  to  see  if  the   infec/on  has  been  cured  acer  treatment.     During  breath  tests  the  pa/ent  is  asked  to  swallow  a  special  substance  that  has  urea  labeled  with  carbon  14.  Urea  is  a  waste   product  the  body  produces  as  it  breaks  down  protein.  The  urea  used  in  the  test  has  been  made  harmlessly  radioac/ve.  If   Helicobacter  pylori  is  present,  the  bacteria  convert  the  urea  into  CO2,  which  is  detected  and  recorded  in  your  exhaled  breath   acer  10  minutes.  This  test  can  iden/fy  almost  all  people  who  have  Helicobacter  pylori.       A  biopsy  may  also  be  taken  from  the  stomach  lining  which  is  the  most  accurate  way  to  tell  if  an  individual  has  Helicobacter   pylori..  To  remove  the  /ssue  sample  the  pa/ent  undergoes  an  endoscopy.       Common  complica/ons  of  helicobacter  pylori  infec/on  are  gastri/s  and  ulcers.  To  check  for  ulcers,  you  may  have  a  special   stomach  x-­‐ray  examina/on  acer  a  barium  meal  which  becomes  visible  on  x-­‐rays.     Next  Slide   10  
  • 11. I  found  it  interes/ng  when  doing  my  research  about  helicobacter  pylori  the  origins  and  geographic  distribu/on   worldwide  affec/ng  50%  of  the  worlds  popula/on  and  genomic  interac/ons  universally.  Helicobacter  pylori  was   first  originated  in  the  African  content  and  mutated  across  the  world  and  has  undergone  gene/c  muta/ons  along   this  spread.  Where  the  old  world  met  the  new  world  the  co-­‐evolu/on  was  disrupted  and  helicobacter  pylori  was   not  dependent  on  infec/ng  host  cells  in  the  African  content.  Individuals  started  to  become  infec/on  with   helicobacter  pylori.  Helicobacter  pylori  encountered  new  gene/c  material  and  evolved  differently  than  compared   to  its  origin.  If  an  individual  did  not  contain  the  resistant  genomic  sequence  to  helicobacter  pylori  it  could  become   cancerous.  Scien/sts  in  Tumaco  Colombia  had  found  the  majority  of  their  DNA  ancestry  and  helicobacter  pylori   strains  come  from  Africa.  The  mountain  popula/on  from  Tuquerres  is  67%  American/Indian  and  31%  European.   Their  helicobacter  pylori  are  mostly  from  European  which  replaced  the  na/ve  strains.  If  the  H.pylori  strains  have  a   different  origin  to  their  hosts,  they  are  more  likely  to  cause  cancer.  Strains  origina/ng  in  Africa  are  mostly  harmless   to  Africans,  but  caused  cancer  in  people  with  a  largely  American/Indian  background     Next  Slide   11  
  • 12. Helicobacter  pylori  is  treated  with  a  double-­‐dose  Proton  pump  inhibitors  such  as  omeprazole,  lansoprazole  and   pantoprazole  which  decreases  the  stomach’s  produc/on  of  acid  allowing  damaged  /ssue  to  heal,  this  is   accompanied  with  2  an/bio/cs  which  increases  treatment  success  and  an/bio/c  resistance.  These  two  an/bio/cs   can  either  be  metronidazole,  clarithromycin  and  amoxicillin     Next  Slide   12  
  • 13. 13  
  • 14. 14  

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