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Incisionless surgery.pptx

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Incisionless surgery.pptx

  1. 1. Tips on using my ppt. 1. You can freely download, edit, modify and put your name etc. 2. Don’t be concerned about number of slides. Half the slides are blanks except for the title. 3. First show the blank slides (eg. Aetiology ) > Ask students what they already know about ethology of today's topic. > Then show next slide which enumerates aetiologies. 4. At the end rerun the show – show blank> ask questions > show next slide. 5. This will be an ACTIVE LEARNING SESSION x three revisions. 6. Good for self study also. 7. See notes for bibliography.
  2. 2. Learning Objectives
  3. 3. Learning Objectives 1. Introduction & History 2. Relevant Anatomy, Physiology 3. Aetiology 4. Pathophysiology 5. Pathology 6. Classification 7. Clinical Features 8. Investigations 9. Management 10. Prevention 11. Guidelines 12. Take home messages
  4. 4. Introduction & History. •
  5. 5. Introduction & History. • The surgical portal to the eradication of diseases, especially malignant diseases, has played a role in longevity. • The surgical incision, our entryway into the body, has allowed for the extirpation of many maladies. • In recent times, the length of the incision has decreased tremendously, allowing for a more effective recovery period. Shorter seems to be better. -
  6. 6. Sharpless Surgery
  7. 7. Sharpless Surgery • Cautery for incision • Clips and staplers for sutures. • Skin staplers for skin closure.
  8. 8. Aetiology
  9. 9. Aetiology • Idiopathic • Congenital/ Genetic • Nutritional Deficiency/excess • Traumatic • Infections /Infestation • Autoimmune • Neoplastic (Benign/Malignant) • Degenerative / lifestyle • Iatrogenic • Psychosomatic • Poisoning/ Toxins/ Drug induced
  10. 10. Etiology of Cancer
  11. 11. Etiology of Cancer • Genetic mutations, whether inherited or sporadic, drive cells toward malignant transformation and degeneration. • The central dogma of genetics, so aptly coined and oversimplified by Francis Crick, is: “DNA makes RNA. RNA makes protein.”
  12. 12. Aetiology of Aetiology •
  13. 13. Aetiology of Aetiology • Idiopathic • Congenital/ Genetic • Nutritional Deficiency/excess • Traumatic • Infections /Infestation • Autoimmune • Neoplastic (Benign/Malignant) • Degenerative / lifestyle • Iatrogenic • Psychosomatic • Poisoning/ Toxins/ Drug induced
  14. 14. Pathophysiology
  15. 15. Pathophysiology • Damaged DNA makes damaged, malfunctioning protein, or makes no protein. • It is this damaged or absent protein that may be the “signature” of the mutant DNA and of cancer.
  16. 16. • The future may be closer than you think. • Proteomics will make this possible.
  17. 17. Proteomics
  18. 18. Proteomics • Proteins are the workhorses of the body, providing cellular structure, facilitating enzymatic activity, helping with molecular transport, and playing critical roles in DNA replication and cellular signaling between cells. In essence, proteins are the locomotives of life.
  19. 19. The Genome, the Proteome
  20. 20. The Genome, the Proteome • The entire set of our genes is the genome. Genes code for the production of proteins. The entire set of our proteins is our proteome, and the study of proteins is termed “proteomics”. • Researchers in the proteomic field study the form and function of our proteins on a large scale. • Often, protein research is combined with the research in genetics, as it is our genes that make our proteins.
  21. 21. Principle
  22. 22. Principle • Working backward, researchers can identify abnormal proteins and attempt to match them with their DNA parent. • It is as if Crick’s central dogma is being reversed: “Protein comes from RNA. RNA comes from DNA.” • First, find the abnormal proteins, and then work toward the mutant parent DNA.
  23. 23. Principle • The protein product is the signature of the gene. • Normal proteins perform the body’s work. Abnormal proteins perform cancer’s work. • Genetically reengineered DNA and modified proteins might perform the surgeon’s work.
  24. 24. Principle • It was recently announced that several unique protein signatures of colorectal cancer have been identified, possibly setting the stage for the eventual early diagnosis and totally noninvasive eradication of colorectal cancer, and by extension, other cancers (Nature 2014;513:382-387).
  25. 25. Principle • Proteomics enabled researchers to isolate abnormal proteins associated with certain subtypes of colorectal cancer. • Further understanding and manipulation of these proteins might enable the IV therapeutic approach, and replace the scalpel in the curative treatment of colorectal cancer. • Or, the therapy could be performed at the DNA level by modifying or repairing mutant DNA.
  26. 26. The Proteomics of Colon Cancer
  27. 27. The Proteomics of Colon Cancer • Beginning in 2005, researchers began cataloging the genetic mutations of those tumors responsible for many of the common cancers. These were published in “The Cancer Genome Atlas” (TCGA). Samples of malignant tumors were collected and their DNA was sequenced, yielding a vast library of tumor DNA genetic sequences.
  28. 28. • Researchers at Vanderbilt University, in Nashville, Tenn., and six other institutions identified five colorectal cancer protein subtypes in the TCGA group (Nature 2014;513:382-387). • Genomic data were integrated with proteomic data.
  29. 29. • Some of the amplified chromosomes in the tumor samples correlated with amplified and abnormal proteins. This suggested that proteomics might yield clues to the most important and common genetic abnormalities, which might be targeted by new “designer” drugs or other therapeutic interventions.
  30. 30. Chromosome 20q.
  31. 31. Chromosome 20q. • Working backward, researchers identified a single chromosome that might contain the responsible colon cancer “driver” genes. For purists, chromosome 20q.
  32. 32. Chromosome 20q. • Chromosome 20, long arm seemed to be associated with three abnormal protein quantities and was associated with corresponding abnormal mRNA. • The genes on chromosome 20q that are thought to be “driver” gene candidates are: HNF4A (hepatocyte nuclear factor 4 ); TOMM34 (translocase of mitochondrial membrane 34); and SRC (SRC proto- oncogene, nonreceptor tyrosine kinase).
  33. 33. Chromosome 20q. • Studies have shown that 20q aberrations do not exist in normal colonic mucosa, appear in some (but not all) of benign adenomas, become more prevalent as colorectal cancer advances and are present in almost all samples of metastatic colorectal cancers.
  34. 34. • The hope is that understanding the structure and functioning of these abnormal proteins will help researchers work backward to find the exact piece of mutated gene responsible for the protein malfunction, and possibly repair the faulty DNA in patients and their at-risk family members. • Barring identification at the DNA level, these proteins might allow for early identification of the dysfunction of our MMR genes or the early identification of malignant disease.
  35. 35. • With constant inspection of our genomic DNA and its protein products, researchers may be on the verge of unlocking the heretofore opaque functioning of our cells and our cellular machinery. • Perhaps incisionless cures will follow soon.
  36. 36. Coming Soon
  37. 37. • The surgeon of tomorrow, after confirming the diagnosis, will don sterile surgical gloves, place an IV line, administer a genetically engineered protein, step away from the patient, grab a cup of coffee and return an hour later to remove the IV line, sending the patient home to recover on the golf course or in a movie theater. Coming Soon
  38. 38. Clinical Features •
  39. 39. Clinical Features • Demography • Symptoms • Signs • Prognosis • Complications
  40. 40. Demography
  41. 41. Demography • Incidence & Prevalence • Geographical distribution. • Race • Age • Sex • Socioeconomic status • Temporal behaviour
  42. 42. Demography • Incidence & Prevalence-
  43. 43. Demography • Geographical distribution.
  44. 44. Demography • Race.
  45. 45. Demography • Age
  46. 46. Demography • Sex
  47. 47. Demography • Socioeconomic status
  48. 48. Demography • Temporal behaviour
  49. 49. Signs
  50. 50. Signs • General Examination • Systemic Examination • Local Examination
  51. 51. Signs • General Examination
  52. 52. Signs • Systemic Examination
  53. 53. Signs • Local Examination
  54. 54. Prognosis
  55. 55. Prognosis • Morbidity • Mortality rate • 5 year survival in Malignancy
  56. 56. Investigations
  57. 57. Investigations • Laboratory Studies – Routine – Special • Imaging Studies • Tissue diagnosis – Cytology • FNAC – Histology – Germ line Testing and Molecular Analysis • Diagnostic Laparotomy.
  58. 58. Investigations in Malignancy •
  59. 59. Investigations in Malignancy • For diagnosis • For staging • For Screening • For Monitoring
  60. 60. Diagnostic Studies
  61. 61. Diagnostic Studies Imaging Studies • X-Ray • USG • CT • Angiography • MRI • Endoscopy • Nuclear scan
  62. 62. Get this ppt in mobile 1. Download Microsoft PowerPoint from play store. 2. Open Google assistant 3. Open Google lens. 4. Scan qr code from next slide.
  63. 63. Get this ppt in mobile
  64. 64. Get my ppt collection • https://www.slideshare.net/drpradeeppande/ edit_my_uploads • https://www.dropbox.com/sh/x600md3cvj8 5woy/AACVMHuQtvHvl_K8ehc3ltkEa?dl =0 • https://www.facebook.com/doctorpradeeppa nde/?ref=pages_you_manage

Notes de l'éditeur

  • drpradeeppande@gmail.com