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Flashcards

Histopathology 3

Alexander Wolff English 200 cards

image of Dukes' classification of colorectal carcinoma

Cards in this deck (200)

  1. 1what screening methods do we have for colorectal cancer?- colonoscopy- indicated for UC/FAP/HNPCC, adenomatous polyps
    - faecal occult bloods
    - flexible sigmoidoscopy
    - genetic testing
  2. 2how can colorectal cancer spread?- direct
    - lymphatic
    - venous (liver, lungs, bones)
  3. 3give some complications of colorectal cancer- obstruction
    - perforation
    - bleeding
    -pericolic abscess
    - fistulae
    - intussusception
  4. 4image of Dukes' classification of colorectal carcinomaimage of Dukes' classification of colorectal carcinoma
  5. 5how does this Dukes classification determine prognosis?class A= 99% 5 year survival
    - class B= 75% 5 year
    - C (C1/2) 35% 5 year survival
  6. 6look at the lecture slides to find out about TNM staging - important also make sure you've looked at survival rates ALL included in the slidesONLY COME BACK WHEN DONE
  7. 7what are the most likely organs to be affected by metastases from colorectal cancer?- lungs
    -liver
  8. 8what mode of inheritance is HNPCC? (also called Lynch syndrome)- autosomal dominant
  9. 9discuss HNPCC- carcinoma develops in younger individuals
    - right sided
    - multiple
    - about 5% of cases of CRC
    - abnormalities in 4 MMR genes (microsatelite instability)
  10. 10what criteria is used to identify HNPCC- the Amsterdam criteria
  11. 11slide showing the Amsterdam criteriaslide showing the Amsterdam criteria
  12. 12what is the prevalence of FAP?- 1 in 8000 individuals
  13. 13what is the prognosis of FAP?without active intervention 100% will develop colon cancer
  14. 14how is FAP characterised?- characterised by multiple polyps throughout the colon
    - polyps not present at birth- develop over time
  15. 15what diagnostic methods do we have for CRC?what diagnostic methods do we have for CRC?
  16. 16where are bone lymphoid precursors generated? remember that this is the primary immune system- thymus
    -bone marrow
  17. 17give examples of the secondary immune system- lymphoid follicle
    -T zone in lymph nodes, spleen, GI tract
  18. 18give two examples of tertiary immunity- the genital tract
    - skin
  19. 19where are stem cells produced for lymphoid tissue?- the bone marrow
  20. 20what do these stem cells differentiate int?- erythoird (RBC), myeloid (WBC)
    - platelets
    - histiocytes
    - lymphoid cells
  21. 21what lineage is a NK cell?- lymphoid
  22. 22how does a B lymphoblast mature into a B lymphocyte?- by rearranging its immunoglobulin genes
    -naive cells exit the bone marrow to enter blood and secondary lymphoid follicles
  23. 23what makes up the B lymphocyte receptor?- immunoglobulin expressed
  24. 24out of interest, what type of animals have immunoglobulin rearrangement in their B cells?- jawed vertebrates
  25. 25why is Ig rearrangement so important?- builds up a large reserve of Ig's and T-cell receptors that are important to fighting pathogens
  26. 26image to show the structure of a secondary- B-cell lymphoid follicle - this is the place of differentiation into a memory B cell or antibody producing plasma cellsimage to show the structure of a secondary- B-cell lymphoid follicle - this is the place of differentiation into a memory B cell or antib...
  27. 27what happens in the germinal centre/- B cells are transformed into centroblasts in an antigen dependent manner
    - centroblasts produce centrocytes, plasma cells and marginal zone B cells (memory B cells)
  28. 28marginal zone B cells are what type of B cell?- memory
  29. 29histology of a reactive lymph node -note the number of lymphoid follicleshistology of a reactive lymph node -note the number of lymphoid follicles
  30. 30what is the largest lymphoid organ committed to local immunity?- Mucosa associated lymphoid tissue
    -found in various organ submucosa
    - well positioned to react quickly to invasion
  31. 31where was MALT first described?- in the peyer's patches (circled in red) of the ileum.where was MALT first described?
  32. 32diagram of MALT - notice: surface epithelium, underlying follicle and T zone - well developed marginal zone - B and T lymphocytes infiltrate surface epitheliumdiagram of MALT - notice: surface epithelium, underlying follicle and T zone - well developed marginal zone - B and T lymphocytes infiltr...
  33. 33what is the role of the tertiary immune system?- mature lymphoid cells that are immune competent patrol surfaces of body in every system
  34. 34describe the process of T cell maturationbegin in the thymis as T lymphoblasts
    - rearrange T cell receptor into alpha beta OR gamma delta
    - these mature into CD4 or CD8 positive cells
    - this whole process is antigen independent
    - exit the thymus as mature T cells
  35. 35name three sources of the secondary immune system- T zone of lymph node
    - MALT
    -spleen
    -requires antigen presenting cells
  36. 36secondary immune systems are antigen dependent true or false?- true
  37. 37give some epidemiology of malignant lymphoma- incidence- gradual rise over the year of 4%
    -nodl 60% and extranodal 40%
    -involves leukaemia and lymphoma
  38. 38what classification system is used for malignant lymphoma?- WHO system
  39. 39how are malignant lymphomas graded ?- on pattern of follicular vs diffuse
    -based on dominant cell type (blastic/cytic)
  40. 40how do we stage malignant lymphoma ?- dependent on the distribution in the body
  41. 41what can malignant lymphoma be caused by medically?- secondary to chemo/radiotherapy (breast cancer for example)
  42. 42what drives malignant lymphoma?-infection/antigen or autoimmune driven
  43. 43what lymphoma is EBV associated with?- Burkitt
    - Hodgkin
    -post transplant/AIDS related
  44. 44what lymphoma is HTLV1 associated with?- T cell non-Hodgkin's
  45. 45what lymphoma is hep c associated with?- low grade B cell non-Hodgkin's
  46. 46what two viruses are associated with plasma cell malignancy?- human herpes virus
    - Kaposi sarcoma virus
  47. 47describe the relationship between malignant lymphoma and the immune systemdescribe the relationship between malignant lymphoma and the immune system
  48. 48a diagram to show pre/inner/post germinal centre neoplasms/lymphomas -B cells onlya diagram to show pre/inner/post germinal centre neoplasms/lymphomas -B cells only
  49. 49NK cells are matured where?-thymus and bone marrow
  50. 50diagram to show T cell lymphoma/ leukaemiadiagram to show T cell lymphoma/ leukaemia
  51. 51describe the WHO classification for lymphomadescribe the WHO classification for lymphoma
  52. 52histology of a low grade B- cell lymphoma involving lymphoid follicles and overactive germinal centre's -note the immuno-staining showing proliferation of B cellshistology of a low grade B- cell lymphoma involving lymphoid follicles and overactive germinal centre's -note the immuno-staining showing...
  53. 53histology of high grade B cell lymphoma -extremely cellularhistology of high grade B cell lymphoma -extremely cellular
  54. 54plasma cell neoplasms are commonly called?- multiple myeloma
  55. 55what feature on radiographs do you see with plasma cell neoplasms/ myeloma?- lytic bony lesions
    -pepperpot skull    what feature on radiographs do you see with plasma cell neoplasms/ myeloma?
  56. 56reminder- plasma cell neoplasms =myeloma
  57. 57image to describe Hodgkin lymphomaimage to describe Hodgkin lymphoma
  58. 58reminder to look for Reed- Sternberg cells in Hodgkin lymphomareminder to look for Reed- Sternberg cells in Hodgkin lymphoma
  59. 59information on the comparison of B- T/NK cell lymphomainformation on the comparison of B- T/NK cell lymphoma
  60. 60what diagnostic methods do we havee for lymphoma/- morphology using H+E staining
    - immunochemistry
    - flow cytometry
    - molecular techniques-PCR/FISH
    - emerging tech
  61. 61example of immunohistochemistry working to identify a follicular lymphoma positive for CD20example of immunohistochemistry working to identify a follicular lymphoma positive for CD20
  62. 62how can we use FISH to aid us with lymphoma?- specific translocations for most cases
    - useful for diagnosis and monitoring
  63. 63list of mature vs precursor B cell lymphomalist of mature vs precursor B cell lymphoma
  64. 64list of mature vs precursor T cell lymphomaslist of mature vs precursor T cell lymphomas
  65. 65defamiliarise yourself with ther layers of the gutdefamiliarise yourself with ther layers of the gut
  66. 66remind yourself of normal oesophageal histology -stratified squamous epitheliumremind yourself of normal oesophageal histology -stratified squamous epithelium
  67. 67describe the trend in age of reflux oesophagitisincreased prevalence with age
    - sharp increase from 30-39    describe the trend in age of reflux oesophagitis
  68. 68list risk factors for reflux oesophagitislist risk factors for reflux oesophagitis
  69. 69picture demonstrating the appearance of reflux oesophagitispicture demonstrating the appearance of reflux oesophagitis
  70. 70histological change seen in reflux oesophagitishistological change seen in reflux oesophagitishistological change seen in reflux oesophagitis
  71. 71name three complications of reflux oesophagitis- stricture
    - Barrett's
    - neoplasia
  72. 72what is oesophageal achalasia?a motility disorder involving the Smooth muscle of the oesophagus and the lower oesophageal sphincter
    -causes sphincter to fail to open when required and remain closed
    -leads to massive dilation of the oesophagus
  73. 73what is the aetiology of achalasia?- autoimmune
  74. 74which cells are affected in achalasia? ?- inflammatory destruction of myenteric ganglion cells
  75. 75name a long term complication of achalasia- squamous cell carcinoma
  76. 76diagram to highlight achalasiadiagram to highlight achalasia
  77. 77histology of achalasia -always remember that this is an infiltration of lymphocytes within the myenteric plexushistology of achalasia -always remember that this is an infiltration of lymphocytes within the myenteric plexus
  78. 78barium swallow and gross anatomy of achalasiabarium swallow and gross anatomy of achalasia
  79. 79name three infective organisms associated with achalasia- candida spp
    - herpes simplex virus
    - trypanosomiasis
  80. 80general appearance of candida with histological appearance in oesophageal tractgeneral appearance of candida with histological appearance in oesophageal tract
  81. 81HSV histology note the existence of eosinophilic intra-nuclear inclusion bodies within ballooned cellsHSV histology note the existence of eosinophilic intra-nuclear inclusion bodies within ballooned cells
  82. 82how is trypanosoma Cruzi transmitted and what is the name of the condition caused?- transmitted in the faeces of blood sucking reduiviid bug- via bite
    - called chagas disease
  83. 83histological appearance of trypanosoma Cruzi infection/Chagas disease examplehistological appearance of trypanosoma Cruzi infection/Chagas disease example
  84. 84to which regions of the world is reduiviid bug endemic?- TAKE TRAVEL HISTORYto which regions of the world is reduiviid bug endemic?
  85. 85what causes pseudo- achalasia ?normally oesophageal malignancy
    -mimics achalasia clinically
  86. 86what is Barrett's metaplasia?- epithelial differentiation change
    - from stratified squamous to simple columnar
    - "metaplastic replacement of oesophageal lining by glandular mucosa"
  87. 87describe the aetiology of Barrett'sreflux of gastric acid and duodenal bile contents into the oesophagus
  88. 88Barrett's on endoscopyBarrett's on endoscopy
  89. 89a schematic diagram of the change that occurs in Barrett's metaplasia note how the squamocolumnar line moves more proximally to the oesophagus -ordinarily to gastrooesophageal junction in line with the squamocolumnar linea schematic diagram of the change that occurs in Barrett's metaplasia note how the squamocolumnar line moves more proximally to the oesop...
  90. 90remind yourself of the normal stratified squamous epithelium of the oesophagus and compare to this image of Barrett's metaplasia - note the columnar epitheliumremind yourself of the normal stratified squamous epithelium of the oesophagus and compare to this image of Barrett's metaplasia - note t...
  91. 91gross anatomy of Barrett's on a specimen -note the squamoucolumnar line being above the gastrooesophageal junctiongross anatomy of Barrett's on a specimen -note the squamoucolumnar line being above the gastrooesophageal junction
  92. 92what can be the progression from Barrett's?- dysplasia
    - followed by adenocarcinoma
  93. 93squamous cell carcinoma accounts for what proportion of oesophageal neoplasia? -describe the epidemiology- 20%
    - M:F= 3:1
    more common in lower>upper>middle
    - China, Japan, iran, South Africa
  94. 94what is the prognosis like for squamous cell carcinoma of the oesophagus?poor
    - treatment with deep X-ray therapy (DXT)
    - surgery indicated
  95. 95adenocarcinoma accounts for how many cases of oesophageal neoplasia?- 80%
    -increasing in prevalence
    - prognosis is good only if caught early
  96. 96remind yourself of the differences between squamous cell carcinoma and adenocarcinomacome back when finished
  97. 97image to show what TNM staging means for oesophageal carcinomaimage to show what TNM staging means for oesophageal carcinoma
  98. 98diagram showing how to classify T (depth) and N- nodal involvementdiagram showing how to classify T (depth) and N- nodal involvement
  99. 99reminder of the anatomy of the stomachreminder of the anatomy of the stomach
  100. 100reminder of the histology of the stomachreminder of the histology of the stomach
  101. 101familiarise/do not learn this table of gastritis classificationsfamiliarise/do not learn this table of gastritis classifications
  102. 102what is the most common form of chronic gastritis (inflammation of stomach lining)chemical / reactive gastritis
  103. 103name one chemical known to cause reactive gastritis- bile
    -reflux from duodenum
  104. 104name drugs that are known to cause chemical/reactive arthritis- aspirin
    - other NSAID's
  105. 105name another chemical that can cause chemical/reactive gastritis- alcohol
  106. 106graphs showing general trend in HP gastritis and reactive gastritis -reactive increasing -HP decreasinggraphs showing general trend in HP gastritis and reactive gastritis -reactive increasing -HP decreasing
  107. 107histology of mild, moderate and severe gastritis -note the increasing cellularityhistology of mild, moderate and severe gastritis -note the increasing cellularity
  108. 108name 4 diseases caused by H. pylori-gastritis
    - ulcers
    - MALT lymphoma
    - carcinoma
  109. 109endoscope image of a case of gastritisendoscope image of a case of gastritis
  110. 110endoscope image of a gastric ulcer H.pyloriendoscope image of a gastric ulcer H.pylori
  111. 111ordinarily, what prevents acid attack from affecting the stomach lining?- mucus secreting cells produce HCO3- and NH4- which act to neutralise H+
    - produces the so-called mucus gel layer
  112. 112how does h.pylori cause gastric disease? -google this nearer the time to understand more fully/mediasite- by releasing LPS
    recruitment of monocytes-production of TNF, IL-1, prostaglandins
    -inflammation by neutrophil recruitment
  113. 113histological comparison of normal vs inflamed gastric mucosa due to H.pyloirhistological comparison of normal vs inflamed gastric mucosa due to H.pyloir
  114. 114histology of a helicobacter associated chronic active gastritishistology of a helicobacter associated chronic active gastritis
  115. 115histology of MALT lymphomahistology of MALT lymphoma
  116. 116how do we treat MALT lymphoma-treat with proton pump inhibitor +- bismuth to get rid of HP
    - regresses MALT
    -therefore the only cancer/lymphoma to be treated with PPI
  117. 117schematic to represent stages of H-pylori related carcinomaschematic to represent stages of H-pylori related carcinoma
  118. 118diagram showing the most common H.pylri cancer sites -most commonly the Antrum/antral junction/GOJ (demarcation between duodenum and stomach)diagram showing the most common H.pylri cancer sites -most commonly the Antrum/antral junction/GOJ (demarcation between duodenum and stom...
  119. 119what bacterial infection is the most common worldwide?- h.pylori infection
    -important to understand that gastric carcinoma is the 2nd leading cause of death worldwide
    -
  120. 120describe the pathogenesis of gastric carcinoma in relation to H.pylori- H.pylori rated as a class 1 carcinogen
    - pathogenesis is complex and multifactorial but key evens triggered by H.pylori
  121. 121gastric carcinoma caused by H.pylorigastric carcinoma caused by H.pylori
  122. 122describe the epidemiology of adenocarcinoma of the stomachm:f of 3:1
    - 7th commonest killer in UK
    - common in Japan, Korea and Chile
  123. 123discuss the risk factors for adenocarcinoma of the stomach- diet (high salt, low dairy)
    -H.pylori and intestinal metaplasia- leads to dysplasia
  124. 124discuss the prognosis of adenocarcinoma of the stomachpoor if advanced (<20%5 year survival)
    good if early (90% 5 year)
  125. 125histology discriminating intestinal-type carcinoma with diffuse-type carcinomahistology discriminating intestinal-type carcinoma with diffuse-type carcinoma
  126. 126gross anatomy of GIST (gastrointestinal stromal tumour)gross anatomy of GIST (gastrointestinal stromal tumour)
  127. 127describe GIST- rare
    - stomach>SI>oesophagus and large bowel
    mutations in the tyrosine kinase genes (KIT)
    -
  128. 128how do we treat GIST-TKI inhibitors such as imatinib
    - surgery
  129. 129ordinary small intestine histologyordinary small intestine histology
  130. 130describe coeliac disease /gluten intolerance- condition of malabsorption (anaemia, low albumin)
    - auto-immune, abnormal immunological reaction to gluten
    - improves with gluten free diet
    - relapse when gluten reintroduced
  131. 131what pathology do we see in coeliac disease?- flattened mucosa
    - reduction in the normal villous height to crypt depth ratio from 5:1 to <3:1
    - crypt hyperplasia
    - increased intraepithelial lymphocytes
    - infiltration of the lamina propria by plasma cells and lymphocytes
  132. 132histology to compare coeliac to normal mucosa -note the flat mucosa and crypt hyperplasia and intraepithelial lymphocyteshistology to compare coeliac to normal mucosa -note the flat mucosa and crypt hyperplasia and intraepithelial lymphocytes
  133. 133image to demonstrate intraepithelial lymphocytes seen in coeliac diseaseimage to demonstrate intraepithelial lymphocytes seen in coeliac disease
  134. 134what is refractory spure?- a complication of coeliac disease
    - where there is a lack of response to gluten restriction- villi do not recover
  135. 135what jejunal complication is associated with coeliac disease?- ulcerative jejunitis
  136. 136name one other complication of coeliac disease- neoplasia
    -e.g. enteropathy-associated T-cell lymphoma (EATL)
    - small intestinal adenocarcinoma
  137. 137describe EATLEnteropathy-associated T-cell lymphoma (EATL) is a rare and usually rapidly fatal intestinal T-cell non-Hodgkin lymphoma. It arises from intraepithelial lymphocytes and has a high association with coeliac disease.
  138. 138gross specimens of EATLgross specimens of EATL
  139. 139histology of EATL -note the prominence of white cytoplasms and large cells with prominent nucleolihistology of EATL -note the prominence of white cytoplasms and large cells with prominent nucleoli
  140. 140what microorganism is responsible for giardiasis?- Giardia lamblia
    - this is the commonest small intestinal protozoal infection WORLDWIDE
  141. 141how is Giardia lamblia spread- through contaminated water (feacal-oral)
  142. 142who are the most at risk for Giardia lamblia infection?- immunocompromised
    - people with AIDS and common variable immunodeficiency
  143. 143describe the histology of Giardia lambliasmall intestinal mucosa either normal OR inflamed
    - can sometimes see the Giardia lamblia    describe the histology of Giardia lamblia
  144. 144name some duodenal causes of adenoma- FAP
  145. 145name some causes of adenocarcinoma in the small intestine (rare)- coeliac disease, crohns, FAP
  146. 146what can cause small intestinal lymphoma?- B cell- burkitt's
    - T cell lymphoma (EATL)
  147. 147just remember that neuro endocrine tumours can cause GI problemsjust remember that neuro endocrine tumours can cause GI problems
  148. 148gross anatomy of neuroscience-endocrine tumours -carcinoids- slow growing neuro endocrine tumourgross anatomy of neuroscience-endocrine tumours -carcinoids- slow growing neuro endocrine tumour
  149. 149research neuro endocrine tumours histologyreturn once completed
  150. 150in what proportion of cases can a high quality post mortem provide the cause of death?- 22-76%
  151. 151why is a post mortem important to families with babies who have died?- need to know why they died
    - important implications to planning and managing future pregnancies
  152. 152what is the current rate of perinatal mortality?-7.4 per 1000 deliveries
    total of 5340 deaths per year
    -stat hasn't really changed over the past 10 years
  153. 153give some indications for perinatal autopsy- termination of pregnancy due to fatal abnormality
    - hydrops fetalis
    - suspected intrauterine infection
    - deaths of twins/higher order multiples
  154. 154what is hydrops fetalis?- accumulation of fluid between 2 or more compartments of the fetus
    -pleural effusion
    - pericardial effusion etc
    leads to oedema
  155. 155list of common reasons for perinatal autopsylist of common reasons for perinatal autopsy
  156. 156what are we looking for in perinatal autopsies? -maceration is the process occurring immediately after fetal death that appears skin dissociation from other tissueswhat are we looking for in perinatal autopsies? -maceration is the process occurring immediately after fetal death that appears skin diss...
  157. 157more pathology to look for -broken ribs, bones etcmore pathology to look for -broken ribs, bones etc
  158. 158in the above example- what is the diagnosis?- skeletal dysplasia
    - shortened and distorted with diffuse bone fractures
    - normal organs and normal placenta
    - OSTEOGENISIS IMPERFECTA
  159. 159what should be done post perinatal autopsy in this example?- because a bony abnormality- x ray
    - bacteriology if clinically indicated/virology
    -karyotyping
    -storage of DNA, biochemistry performed and haematology
    -ONLY IF CLINICALLY INDICATED
  160. 160what is the most common obstetric event that leads to perinatal death?- spontaneous preterm delivery
    AND
    -hypertensive disorders
    (28.7%)
  161. 161what is the most common cause of early neonatal death?- prematurity
    62%
  162. 162what proportion of fetal deaths are associated with fetal abnormalities?- only 12%
  163. 163what is: 1)trisomy 21 2)trisomy 18 3)trisomy 13 4) triploidy 5)Turner's syndrome1)Down's (1 per 800)
    2) Edward's
    3) Patau's
    5) 45/X0
  164. 164image of the clinical features of trisomy 21image of the clinical features of trisomy 21
  165. 165describe why babies born to mothers with diabetes are at higher risk of perinatal death- increased somatic size (macrosomia)
    - increased incidence of perinatal death)
    - increased frequency of malformation
    - hypertrophy of islets of Langerhans with B cells hyperplasia
  166. 166how does pre-eclampsia present clinically (known to cause perinatal death)- maternal high blood pressure
    AND
    protein found in urine
  167. 167what common findings are there with pre-eclampsia related perinatal autopsy?- intra-uterine growth restriction
    - asymmetrical growth
  168. 168what other reasons are there for pre-eclampsia?- maternal drug abuse
    - thrombophilia
    - autoimmune disorders
    - malformed uterus (growth restriction)
  169. 169picture of two common pathological findings in perinatal autopsiespicture of two common pathological findings in perinatal autopsies
  170. 170what two neural tube defects are also common findings in perinatal autopsy?what two neural tube defects are also common findings in perinatal autopsy?
  171. 171more examples of common pathologies in perinatal autopsymore examples of common pathologies in perinatal autopsy
  172. 172more examples of common pathologies in perinatal autopsymore examples of common pathologies in perinatal autopsy
  173. 173what is oligohydramnios?-Oligohydramnios is a condition in pregnancy characterized by a deficiency of amniotic fluid
  174. 174symptoms of SIADH?-polyuria
    -polydipsia
  175. 175what placenta pathology is common in pre-eclampsia?- IUGR and placental infarctwhat placenta pathology is common in pre-eclampsia?
  176. 176what is acute choriomanionitis?- acute inflammation of the fetal membranes
    -common after PROM
    - can be caused by ascending infection
  177. 177what is PROMpremature rupture of membranes
    - ordinarily occurs where membranes rupture- amniotic fluid leaks- water broken (pre-labour)
    -PROM- at least 1 hour before onset of labour
  178. 178what is clinico-pathological correlation and why is it important in perinatal autopsy- objective summary and correlation of clinical findings with results of other autopsies
    - to describe the death and sequence of events leading to death
    - a discussion/listing of the possible cause included.
  179. 179list of most common childhood cancerslist of most common childhood cancers
  180. 180what is a Wilms tumoura tumour of the kidneys
    -also called a nephroblastoma
  181. 181describe the aetiology of childhood cancers- normally a genetic change very early in life (can be before birth)
    - not strongly linked to lifestyle or environmental risk factors
  182. 182some general information about childhood cancer treatmentsome general information about childhood cancer treatment
  183. 183describe Hirschsprung's disease- a developmental disorder with absence of ganglion cells in distal rectum
    -the Aganglionic length is of variable length
  184. 184how is Hirschsprung's caused?- failure of neural crest cells to migrate
    -during development of enteric nervous system
  185. 185Hirschsprung's is genetically....heterogenous
  186. 186how common is Hirschsprung's?- 1 in 5000 births
  187. 187what proportion of Hirschsprung's are syndromic?- 30%
  188. 188which sex suffers most from Hirschsprung's?- males 4:1
  189. 189how does Hirschsprung's present?- normally in the newborn period
    - delayed meconium passage
    - abdominal distension
    - billous vomiting
  190. 190what is the prognosis if treatment is not given for Hirschsprung's?can cause serious complications
    -given surgery and reanastomosis
  191. 191histology comparing fully ganglionic normal nerve trunks vs aganglionic nerve trunks in Hirschsprung'shistology comparing fully ganglionic normal nerve trunks vs aganglionic nerve trunks in Hirschsprung's
  192. 192what is the genetic cause of cystic fibrosis>autosomal recessive mutation of the CFTR gene
    -three base loss leading to loss of phenylalanine residue
  193. 193give a brief description of the pathology of CF- mucus plugging of airways
    - severe suppurative lung disease (pus production)
    - leads to bronchiectasis
  194. 194some of the complications of CFsome of the complications of CF
  195. 195what bowel complications exist for CF?- 15% have some bowel involvement
    - bowel lump filled with inspissated meconium
    - can have intestinal atresia
    - rectal prolaps
  196. 196image of meconium ileus - this happens in CF and can cause severe blockages of the ileumimage of meconium ileus - this happens in CF and can cause severe blockages of the ileum
  197. 197histology of CF demonstrating deep mucus extension into the crypts (arrow)histology of CF demonstrating deep mucus extension into the crypts (arrow)
  198. 198in children- coeliac disease is caused by what?- T cell response in small intestine
    -inflammatory reaction to gliadine- component of gluten
    -incidence of 1:100
  199. 199name two conditions which increase incidence of coeliac disease- insulin dependent diabetes
    - trisomy 21
  200. 200what two factors might reduce risk of coeliac disease?- breastfeeding
    - early introduction (<4 months)

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Flashcards on Histopathology 3, created by Alexander Wolff on 04/11/2017.
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