Karteikarten
Histopathology 3
Karten in diesem Stapel (200)
- 1what screening methods do we have for colorectal cancer?- colonoscopy- indicated for UC/FAP/HNPCC, adenomatous polyps
- faecal occult bloods
- flexible sigmoidoscopy
- genetic testing - 2how can colorectal cancer spread?- direct
- lymphatic
- venous (liver, lungs, bones) - 3give some complications of colorectal cancer- obstruction
- perforation
- bleeding
-pericolic abscess
- fistulae
- intussusception - 4image of Dukes' classification of colorectal carcinoma
- 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 - 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
- 7what are the most likely organs to be affected by metastases from colorectal cancer?- lungs
-liver - 8what mode of inheritance is HNPCC? (also called Lynch syndrome)- autosomal dominant
- 9discuss HNPCC- carcinoma develops in younger individuals
- right sided
- multiple
- about 5% of cases of CRC
- abnormalities in 4 MMR genes (microsatelite instability) - 10what criteria is used to identify HNPCC- the Amsterdam criteria
- 11slide showing the Amsterdam criteria
- 12what is the prevalence of FAP?- 1 in 8000 individuals
- 13what is the prognosis of FAP?without active intervention 100% will develop colon cancer
- 14how is FAP characterised?- characterised by multiple polyps throughout the colon
- polyps not present at birth- develop over time - 15what diagnostic methods do we have for CRC?
- 16where are bone lymphoid precursors generated? remember that this is the primary immune system- thymus
-bone marrow - 17give examples of the secondary immune system- lymphoid follicle
-T zone in lymph nodes, spleen, GI tract - 18give two examples of tertiary immunity- the genital tract
- skin - 19where are stem cells produced for lymphoid tissue?- the bone marrow
- 20what do these stem cells differentiate int?- erythoird (RBC), myeloid (WBC)
- platelets
- histiocytes
- lymphoid cells - 21what lineage is a NK cell?- lymphoid
- 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 - 23what makes up the B lymphocyte receptor?- immunoglobulin expressed
- 24out of interest, what type of animals have immunoglobulin rearrangement in their B cells?- jawed vertebrates
- 25why is Ig rearrangement so important?- builds up a large reserve of Ig's and T-cell receptors that are important to fighting pathogens
- 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 cells
- 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) - 28marginal zone B cells are what type of B cell?- memory
- 29histology of a reactive lymph node -note the number of lymphoid follicles
- 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 - 31where was MALT first described?- in the peyer's patches (circled in red) of the ileum.
- 32diagram of MALT - notice: surface epithelium, underlying follicle and T zone - well developed marginal zone - B and T lymphocytes infiltrate surface epithelium
- 33what is the role of the tertiary immune system?- mature lymphoid cells that are immune competent patrol surfaces of body in every system
- 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 - 35name three sources of the secondary immune system- T zone of lymph node
- MALT
-spleen
-requires antigen presenting cells - 36secondary immune systems are antigen dependent true or false?- true
- 37give some epidemiology of malignant lymphoma- incidence- gradual rise over the year of 4%
-nodl 60% and extranodal 40%
-involves leukaemia and lymphoma - 38what classification system is used for malignant lymphoma?- WHO system
- 39how are malignant lymphomas graded ?- on pattern of follicular vs diffuse
-based on dominant cell type (blastic/cytic) - 40how do we stage malignant lymphoma ?- dependent on the distribution in the body
- 41what can malignant lymphoma be caused by medically?- secondary to chemo/radiotherapy (breast cancer for example)
- 42what drives malignant lymphoma?-infection/antigen or autoimmune driven
- 43what lymphoma is EBV associated with?- Burkitt
- Hodgkin
-post transplant/AIDS related - 44what lymphoma is HTLV1 associated with?- T cell non-Hodgkin's
- 45what lymphoma is hep c associated with?- low grade B cell non-Hodgkin's
- 46what two viruses are associated with plasma cell malignancy?- human herpes virus
- Kaposi sarcoma virus - 47describe the relationship between malignant lymphoma and the immune system
- 48a diagram to show pre/inner/post germinal centre neoplasms/lymphomas -B cells only
- 49NK cells are matured where?-thymus and bone marrow
- 50diagram to show T cell lymphoma/ leukaemia
- 51describe the WHO classification for lymphoma
- 52histology of a low grade B- cell lymphoma involving lymphoid follicles and overactive germinal centre's -note the immuno-staining showing proliferation of B cells
- 53histology of high grade B cell lymphoma -extremely cellular
- 54plasma cell neoplasms are commonly called?- multiple myeloma
- 55what feature on radiographs do you see with plasma cell neoplasms/ myeloma?- lytic bony lesions
-pepperpot skull
- 56reminder- plasma cell neoplasms =myeloma
- 57image to describe Hodgkin lymphoma
- 58reminder to look for Reed- Sternberg cells in Hodgkin lymphoma
- 59information on the comparison of B- T/NK cell lymphoma
- 60what diagnostic methods do we havee for lymphoma/- morphology using H+E staining
- immunochemistry
- flow cytometry
- molecular techniques-PCR/FISH
- emerging tech - 61example of immunohistochemistry working to identify a follicular lymphoma positive for CD20
- 62how can we use FISH to aid us with lymphoma?- specific translocations for most cases
- useful for diagnosis and monitoring - 63list of mature vs precursor B cell lymphoma
- 64list of mature vs precursor T cell lymphomas
- 65defamiliarise yourself with ther layers of the gut
- 66remind yourself of normal oesophageal histology -stratified squamous epithelium
- 67describe the trend in age of reflux oesophagitisincreased prevalence with age
- sharp increase from 30-39
- 68list risk factors for reflux oesophagitis
- 69picture demonstrating the appearance of reflux oesophagitis
- 70histological change seen in reflux oesophagitis
- 71name three complications of reflux oesophagitis- stricture
- Barrett's
- neoplasia - 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 - 73what is the aetiology of achalasia?- autoimmune
- 74which cells are affected in achalasia? ?- inflammatory destruction of myenteric ganglion cells
- 75name a long term complication of achalasia- squamous cell carcinoma
- 76diagram to highlight achalasia
- 77histology of achalasia -always remember that this is an infiltration of lymphocytes within the myenteric plexus
- 78barium swallow and gross anatomy of achalasia
- 79name three infective organisms associated with achalasia- candida spp
- herpes simplex virus
- trypanosomiasis - 80general appearance of candida with histological appearance in oesophageal tract
- 81HSV histology note the existence of eosinophilic intra-nuclear inclusion bodies within ballooned cells
- 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 - 83histological appearance of trypanosoma Cruzi infection/Chagas disease example
- 84to which regions of the world is reduiviid bug endemic?- TAKE TRAVEL HISTORY
- 85what causes pseudo- achalasia ?normally oesophageal malignancy
-mimics achalasia clinically - 86what is Barrett's metaplasia?- epithelial differentiation change
- from stratified squamous to simple columnar
- "metaplastic replacement of oesophageal lining by glandular mucosa" - 87describe the aetiology of Barrett'sreflux of gastric acid and duodenal bile contents into the oesophagus
- 88Barrett's on endoscopy
- 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 line
- 90remind yourself of the normal stratified squamous epithelium of the oesophagus and compare to this image of Barrett's metaplasia - note the columnar epithelium
- 91gross anatomy of Barrett's on a specimen -note the squamoucolumnar line being above the gastrooesophageal junction
- 92what can be the progression from Barrett's?- dysplasia
- followed by adenocarcinoma - 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 - 94what is the prognosis like for squamous cell carcinoma of the oesophagus?poor
- treatment with deep X-ray therapy (DXT)
- surgery indicated - 95adenocarcinoma accounts for how many cases of oesophageal neoplasia?- 80%
-increasing in prevalence
- prognosis is good only if caught early - 96remind yourself of the differences between squamous cell carcinoma and adenocarcinomacome back when finished
- 97image to show what TNM staging means for oesophageal carcinoma
- 98diagram showing how to classify T (depth) and N- nodal involvement
- 99reminder of the anatomy of the stomach
- 100reminder of the histology of the stomach
- 101familiarise/do not learn this table of gastritis classifications
- 102what is the most common form of chronic gastritis (inflammation of stomach lining)chemical / reactive gastritis
- 103name one chemical known to cause reactive gastritis- bile
-reflux from duodenum - 104name drugs that are known to cause chemical/reactive arthritis- aspirin
- other NSAID's - 105name another chemical that can cause chemical/reactive gastritis- alcohol
- 106graphs showing general trend in HP gastritis and reactive gastritis -reactive increasing -HP decreasing
- 107histology of mild, moderate and severe gastritis -note the increasing cellularity
- 108name 4 diseases caused by H. pylori-gastritis
- ulcers
- MALT lymphoma
- carcinoma - 109endoscope image of a case of gastritis
- 110endoscope image of a gastric ulcer H.pylori
- 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 - 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 - 113histological comparison of normal vs inflamed gastric mucosa due to H.pyloir
- 114histology of a helicobacter associated chronic active gastritis
- 115histology of MALT lymphoma
- 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 - 117schematic to represent stages of H-pylori related carcinoma
- 118diagram showing the most common H.pylri cancer sites -most commonly the Antrum/antral junction/GOJ (demarcation between duodenum and stomach)
- 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
- - 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 - 121gastric carcinoma caused by H.pylori
- 122describe the epidemiology of adenocarcinoma of the stomachm:f of 3:1
- 7th commonest killer in UK
- common in Japan, Korea and Chile - 123discuss the risk factors for adenocarcinoma of the stomach- diet (high salt, low dairy)
-H.pylori and intestinal metaplasia- leads to dysplasia - 124discuss the prognosis of adenocarcinoma of the stomachpoor if advanced (<20%5 year survival)
good if early (90% 5 year) - 125histology discriminating intestinal-type carcinoma with diffuse-type carcinoma
- 126gross anatomy of GIST (gastrointestinal stromal tumour)
- 127describe GIST- rare
- stomach>SI>oesophagus and large bowel
mutations in the tyrosine kinase genes (KIT)
- - 128how do we treat GIST-TKI inhibitors such as imatinib
- surgery - 129ordinary small intestine histology
- 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 - 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 - 132histology to compare coeliac to normal mucosa -note the flat mucosa and crypt hyperplasia and intraepithelial lymphocytes
- 133image to demonstrate intraepithelial lymphocytes seen in coeliac disease
- 134what is refractory spure?- a complication of coeliac disease
- where there is a lack of response to gluten restriction- villi do not recover - 135what jejunal complication is associated with coeliac disease?- ulcerative jejunitis
- 136name one other complication of coeliac disease- neoplasia
-e.g. enteropathy-associated T-cell lymphoma (EATL)
- small intestinal adenocarcinoma - 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.
- 138gross specimens of EATL
- 139histology of EATL -note the prominence of white cytoplasms and large cells with prominent nucleoli
- 140what microorganism is responsible for giardiasis?- Giardia lamblia
- this is the commonest small intestinal protozoal infection WORLDWIDE - 141how is Giardia lamblia spread- through contaminated water (feacal-oral)
- 142who are the most at risk for Giardia lamblia infection?- immunocompromised
- people with AIDS and common variable immunodeficiency - 143describe the histology of Giardia lambliasmall intestinal mucosa either normal OR inflamed
- can sometimes see the Giardia lamblia
- 144name some duodenal causes of adenoma- FAP
- 145name some causes of adenocarcinoma in the small intestine (rare)- coeliac disease, crohns, FAP
- 146what can cause small intestinal lymphoma?- B cell- burkitt's
- T cell lymphoma (EATL) - 147just remember that neuro endocrine tumours can cause GI problems
- 148gross anatomy of neuroscience-endocrine tumours -carcinoids- slow growing neuro endocrine tumour
- 149research neuro endocrine tumours histologyreturn once completed
- 150in what proportion of cases can a high quality post mortem provide the cause of death?- 22-76%
- 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 - 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 - 153give some indications for perinatal autopsy- termination of pregnancy due to fatal abnormality
- hydrops fetalis
- suspected intrauterine infection
- deaths of twins/higher order multiples - 154what is hydrops fetalis?- accumulation of fluid between 2 or more compartments of the fetus
-pleural effusion
- pericardial effusion etc
leads to oedema - 155list of common reasons for perinatal autopsy
- 156what are we looking for in perinatal autopsies? -maceration is the process occurring immediately after fetal death that appears skin dissociation from other tissues
- 157more pathology to look for -broken ribs, bones etc
- 158in the above example- what is the diagnosis?- skeletal dysplasia
- shortened and distorted with diffuse bone fractures
- normal organs and normal placenta
- OSTEOGENISIS IMPERFECTA - 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 - 160what is the most common obstetric event that leads to perinatal death?- spontaneous preterm delivery
AND
-hypertensive disorders
(28.7%) - 161what is the most common cause of early neonatal death?- prematurity
62% - 162what proportion of fetal deaths are associated with fetal abnormalities?- only 12%
- 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 - 164image of the clinical features of trisomy 21
- 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 - 166how does pre-eclampsia present clinically (known to cause perinatal death)- maternal high blood pressure
AND
protein found in urine - 167what common findings are there with pre-eclampsia related perinatal autopsy?- intra-uterine growth restriction
- asymmetrical growth - 168what other reasons are there for pre-eclampsia?- maternal drug abuse
- thrombophilia
- autoimmune disorders
- malformed uterus (growth restriction) - 169picture of two common pathological findings in perinatal autopsies
- 170what two neural tube defects are also common findings in perinatal autopsy?
- 171more examples of common pathologies in perinatal autopsy
- 172more examples of common pathologies in perinatal autopsy
- 173what is oligohydramnios?-Oligohydramnios is a condition in pregnancy characterized by a deficiency of amniotic fluid
- 174symptoms of SIADH?-polyuria
-polydipsia - 175what placenta pathology is common in pre-eclampsia?- IUGR and placental infarct
- 176what is acute choriomanionitis?- acute inflammation of the fetal membranes
-common after PROM
- can be caused by ascending infection - 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 - 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. - 179list of most common childhood cancers
- 180what is a Wilms tumoura tumour of the kidneys
-also called a nephroblastoma - 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 - 182some general information about childhood cancer treatment
- 183describe Hirschsprung's disease- a developmental disorder with absence of ganglion cells in distal rectum
-the Aganglionic length is of variable length - 184how is Hirschsprung's caused?- failure of neural crest cells to migrate
-during development of enteric nervous system - 185Hirschsprung's is genetically....heterogenous
- 186how common is Hirschsprung's?- 1 in 5000 births
- 187what proportion of Hirschsprung's are syndromic?- 30%
- 188which sex suffers most from Hirschsprung's?- males 4:1
- 189how does Hirschsprung's present?- normally in the newborn period
- delayed meconium passage
- abdominal distension
- billous vomiting - 190what is the prognosis if treatment is not given for Hirschsprung's?can cause serious complications
-given surgery and reanastomosis - 191histology comparing fully ganglionic normal nerve trunks vs aganglionic nerve trunks in Hirschsprung's
- 192what is the genetic cause of cystic fibrosis>autosomal recessive mutation of the CFTR gene
-three base loss leading to loss of phenylalanine residue - 193give a brief description of the pathology of CF- mucus plugging of airways
- severe suppurative lung disease (pus production)
- leads to bronchiectasis - 194some of the complications of CF
- 195what bowel complications exist for CF?- 15% have some bowel involvement
- bowel lump filled with inspissated meconium
- can have intestinal atresia
- rectal prolaps - 196image of meconium ileus - this happens in CF and can cause severe blockages of the ileum
- 197histology of CF demonstrating deep mucus extension into the crypts (arrow)
- 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 - 199name two conditions which increase incidence of coeliac disease- insulin dependent diabetes
- trisomy 21 - 200what two factors might reduce risk of coeliac disease?- breastfeeding
- early introduction (<4 months)
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- Karteikarten am Histopathology 3, erstellt von Alexander Wolff am 04/11/2017.
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