Glossary of pathology final
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- CD10 lymphoma type
- marrow pre-B, germinal center B
- CD19, CD20 lymphoma type
- marrow pre B; mature B (not plasma)
- CD21 lymphoma type
- EBV-receptor on mature B
- CD23 lymphoma type
- activated, mature B
- CD2, CD3 lymphoma type
- CD5 lymphoma type
- T and some B
- CD4, CD8 lymphoma type
- sets of T
- CD7 lymphoma type
- earliest T cell specific
- Follicular B cell lymphoma; patient type, prognosis
- >40, F
5-8 years survival
50% -> aggressive large cell lymphomas
- Follicular B cell lymphoma sx
- painless adenopathy
most present w/ advance
(multiple nodes and bone marrow)
- follicular B cell genetic pathogenesis
- 85% have 14-18 translocation with overexpression of BCL2-->poor chemo response
- follicular B cell lymphoma cleaved cell histo appearance
- small irregular lymphocytes w/ low cytoplasm
- follicular b cell lymphoma large follicular center cells histo appearance
- more cytoplasm than cleaved
dispersed chromatin, multiple nuclei (NO FOLLICLES)
- follicular B cell lymphomas surface antigens
- abundant surface IgM>>IgG>IgA (stain kappa or lambda)
B cells: CD5-, CD10+, CD19+, CD20+
- Diffuse large B cell lymphoma epidemiology
- Most common lymphoma
adults ~60, M
children possible, aggressive
- Diffuse large B cell lymphoms clinical presentation
- Rapidly enlarging mass
node based, w/ 40% extranodal (GI, CNS, Bone)
- Diffuse large B cell lymphomas genetic pathogenesis, prognosis
- 30% have 14-18 translocation; may arise from Follicular B Cell Lymphoma
70% have other abnormality
the more aggresssive, the more curable
- Diffuse Large B Cell Lymphoma histo appearance
- Diffuse growth
Large lymphocytes with big nuclei
- Diffuse Large B cell surface antigens
- Surface Ig
B cell Lymphoma
- Most aggressive
Endemic in africa (w/ EBV)
Sporadic in US
- Burkitt's B cell lymphoma clinical
- Big lump
Extranodal disease (jaw/facial bone in africa), GI (all types)
- Burkitt's B cell lymphoma genetic pathogenesis, prognosis
- translocation of heavy chain (chr 14) or light chain (k chr 22, or l chr 22) to c-myc (chr8)
--> uncontrolled growth
chemosensitive, 90% cure
- burkitt's b cell lymphona histo appearance
- diffuse growth pattern, starry sky (macrophages)
Small, blast like B cells, dispersed chromatin
Very high mitosis
- Burkitt's b cell lymphoma surface antigens
- abundant surface IgM>>IgG
- extranodal MALT B cell lymphoma; epidemiology,
- adults in their 60s
- Extranodal MALT B cell lymphoma clinical appearance
painless mass lesion
- Extranodal MALT B Cell Lymphoma genetic pathogenesis
- trisomy 3 or 11-18 translocation
NO BCL2 or c-myc translocations
- Extranodal MALT B cell lymphoma histological appearance
- Diffuse infiltrate invades epithelial structures
Small/medium lymphocytes, abundant cytoplasm
plasma cell component possible
- Extranodal MALT B cell lymphoma surface antigens
- CD5-; CD10-; CD23-
- T cell lymphomas epidemiology and prognosis
- 15% of NHLs (85% B cells)
More aggressive than B cells; difficult to diagnose, younger patients
- T cell lymphomas paraneoplastic syndromes
- hypercalcemia, hypergammaglobulinemia, erythrophagocytosis
- Where to T cell lymphomas arise?
- peripheral sites (not thymus)
- T cell lymphoma surface antigens that may be lost
- CD2, CD3, or CD7
- T cell lymphoblastic lymphoma/leukemia typical patients, prognosis
- young males
80% cure rate
- t cell lymphoblastic lymphoma/leukemia clinical presentation
- rapidly growing mediastinal mass
- T cell lymphoblastic lymphoma/leukemia histological appearance
- immature t cell blasts(x2 RBC)
starry sky; frequent mitosis;
invasion of thymic capsule
high N:C ratio; folded nuclei, fine chromatin, nucleoli not obvious
- T cell lymphoblastic lymphoma/leukemia surface antigens
CD2+; CD7+; CD4/CD8/CD3 +/-
- T Cell mycosis fungoides and sezary syndrome epidemiology and prognosis
- 40s M
May progress to large cell lymphoma with poor prognisis
- T cell mycosis fungoides and sezary syndrome clinical presentation
erythematous, pruritic skin lesions in sun protected areas (patch -> plaque -> tumor)
erythroderma; circulating tumor cells, generalized lymphadenopathy
- T cell mycosis fungoides and sezary syndrome histological appearance
- small t cells; initially forming mild perivascular infiltrates (pautrier's microabscess)
Sezary cell (nucleus looks like a labyrinth)
at transformation cells become large
- Peripheral T cell lymphoma unspecified epidemiology
- Adults, sometimes children
50% of all peripheral t cells in western world
- peripheral t cell lymphoma clinical appearance
Can spread to BM, liver, spleen, skin
Circulating tumor cells
Paraneoplastic (eosinophilia, pruritis, hemophagocytosis)
- peripheral t cell lymphoma unspecified histological appearance
- pleomorphic mix of small/medium/large mature T cells
Effaced nodal architecture
Loss of a surface marker
Circulating cells: "clover leaf" appearance
- Anaplastic Large T Cell Lymphoma epidemiology
- most common peripheral lymphoma of kids, adults
- Anaplastic Large T cell lymphoma clinical appearance
- Peripheral adenopathy
Clean in mediastinum
Extranodal to skin, not marrow
- Anaplastic Large T Cell Lymphoma genetic pathogenesis
- translocation 2:5 dysregulation of tyrosine kinase ALK (anaplastic lymphoma kinase)
- anaplastic large t cell lymphoma histological appearance
- Pleomorphic large cell infiltrate
Effacement of nodal sinuses
- Anaplastic Large T Cell Lymphoma surface antigens
- Epidemiology of Hodgkin's Lymphoma Epidemiology
- 15% of all lymphomas; predominantly b cells
- Nodular sclerosing hodgkins 'classic' patient
- young females
- nodular sclerosing hodgkins clinical presentation
- Cervical lymphadenopathy
30% B symptoms
- Nodular sclerosis hodgkins type of Reed-Sternberg cell
- Lacunar RS; appear to sit within a space
- Nodular sclerosis hodgkins surface antigens
- CD45-; No B/T antigens
CD 15+, CD30+
- Nodular sclerosing Hodgkins histological appearance
- Capsular fibroids made of thick collagenous fibers
Effaced architecture, nodular appearance due to collagen
Abundant reactive cells, scattered lacunar RS variants
- Mixed cellularity Hodgkins epidemiology
- 2nd most common HL; young men; 75% EBV infections
- Mixed cellularity hodgkins clinical presentation
- B symptoms
Involvement of multiple node groups
- Mixed cellularity hodgkin's type of Reed sternberg cell
- Diagnostic RS cells are large binucleate cells, with dispersed nuclear chromatin large nucleoli, and abundant cytoplasm
- Mixed cellularity hodgkin's histological appearance
- Complete nodal effacement
diagnostic RS cells
- Mixed cellularity hodgkins surface antigens
- CD45-; no b/t antigens
- Lymphocyte Rich hodgkins epidemiology
- 5% of HL; adult men
- Lymphocyte rich hodgkins clinical presentation
- peripheral adenopathy
no b symptoms
- Lymphocyte rich hodgkins distinctive cells
- Lymphocyte and histiocyte RS cells have polylobulated nuclei (popcorn cells)
Immunophenotype is that of diagnostic RS cells
- lymphocyte rich hodgkins surface antigens
- CD45-; no B/T antigens
- Lymphocyte rich hodgkins histological appearance
- small lymphocytes
Lymphocyte and histiocyte morphology RS cells (popcorn)
- Lymphocyte depleted hodgkins epidemiology
- lymphocyte depleted hodgkins clinical presentation
- B symptoms
Widely dissemitated at presentation
- Lymphocyte depleted hodgkins RS cells
- Diagnostic to bizzare (multinucleated) RS cells
- Lymphocyte depleted hodgkins histological appearance
- RS cells predominant
- Which Hodgkins lymphoma is not classic
- Nodular lymphocyte predominant hodgkins
- nodular lymphocyte predominant hodgkins epidemiology
- Nodular lymphocyte predominant hodgkins clinical presentation
- cervical axillary adenopathy
unstable, may progress to large b cell lymphomas
- nodular lymphocyte predominant hodgkins RS cells
- lymphocyte and histiocyte RS cells
- lymphocyte and histiocyte RS cell antigens
- CD45+; CD20+ (b cell marker)
- nodular lymphocyte predominant hodgkins histological appearance
- mostly small B lymphocytes
Abundant reactive cells
- leukemia w/ CD13
- im/mature monocytes, granulocytes
- leukemia w/ CD14
- leukemia w/ CD15
- granulocytes, RS cells
- leukemia w/ CD33
- myeloid progenitors, monocytes
- leukemia w/ CD34
- pluripotent hematopoietic stem cells
- leukemia w/ CD64
- mature myeloid cells
- leukemia w/ CD45
- all leukocytes
- leukemia w/ CD30
- activated B/T, RS
- Acute myeloid leukemia epidemiology
- 85% of adult acute leukemia
MDR-AML--older, poor prog
DN-AML: younger, better. Poor chem resp
- acute myeloid leukemia clinical presentation
- marrow failure (cytopenias)
- Acute myeloid leukemia genetics
- DN-AML have common translocations:
8:21 (AML1/ETO), 15:17 (PML/RARa)
MDR-AML: background MDS, hypersensitivity to chemo. can't do BMT b/c of age
- Acute myeloid leukemia histological appearance
- Hypercellular marrow, monomorphic blasts
myeloblasts have delicate chromatin
prominent nuclei, fine granules in the pale cytoplasm
- acute myeloid leukemia laboratory diagnosis
- sudan black+
myeloid ags: CD34+, CD13+, CD33+, CD64+
- acute myeloid leukemia tx
- DN-AML responds to cytotoxic chemo. if relapse, BM transplant if young pt
- AML: Acute promyelocytic leukemia epidemiology
- 10% of AML
- AML: acute promyelocytic leukemia biochemical pathology
- Fusion of RAR and PML results in prevention of cells from maturation by not allowing the repressor to be displaced by histone deacytelase complex. Pharm (RA) can remove inhibitor.
Additional mutation in Flt3 causes continuous proliferation through RAS
- AML: acute promyelocytic leukemia histological appearance/lab diagnosis
- dysplastic promyleocytes w/ coarse granules, some have bilobed nuclei, some have Auer rods
High RAR&PML [RA]
- Acute lymphoblastic leukemia epidemiology
- 85% of childhood leukemias
mostly b cells
- acute lymphoblastic leukemia clinical presentation
- mediastinal mass in a young male
relapse in testis and cns
- acute lymphoblastic leukemia histo appearance
- hypercellular marrow
lymphoblasts have little cytoplasm, packed chromatin, few nucleoli, no granules, indented nuclei
- acute lymphoblastic leukemia laboratory diagnosis
- - Sudan Black -, Esterase -, MPO -
- T cells ~ avg prognosis (TdT+, CD2+, CD7+)
- B cells (TEL/AML1) – good – less chemo - kids
-(BCR/ABL) – poor – more chemo - adults
(CD19+, CD10+, TdT+)
- Chronic Lymphocytic Leukemia
- Most common in western world.
Indolent, 7 y
- Chronic Lymphocytic Leukemia
- - Often asymptomatic
- Anemia, infections
- Hepatosplenomegaly, lymphadenopathy
- WBC 10K – 300K
- Chronic Lymphocytic Leukemia
- Mutated Ig V genes better prognosis. Cytogenic abnormalities: trisomy 12, del 13q14, del 11q22-23 present. Prolymphocytic – larger lymphocytes with a nucleolus transf (15-30%), Richter – large B cell lymphoma- transf (10%)
- Chronic Lymphocytic Leukemia
- - Lymphocytosis (>10K), anemia, thrombocytopenia.
- Peripheral: Small lymphocytes (slightly larger than normal resting lymphocytes) & smudge cells.
- BM: diffuse or nodular inf. Small lymphocytes
- LN: proliferation centers, randomly arranged
- Chronic Lymphocytic Leukemia
- - B cells : CD20 +, CD5+ (which is a T cell marker), CD23+, monotypic surface Ig.
- almost never T cells
- Hairy Cell Leukemia
- Rare, 55 y. M
- hairy cell leukemia clinical presentation/complications
- - Splenomegaly early satiety
- Pancytopenia w/ very serious monocytopenia
- Recurrent infections
- hairy cell leukemia histological appearance, lab dx
- - Peripheral: Lymphocytes with villous protrusions
- Spleen: RP infiltrates
- B cells: CD20+, CD103+, CD11c+, CD25+, monotypic surface Ig
- hairy cell leukemia tx
- nucleotide analog therapy (2-CDA), prolonged complete remissions
- chronic myelogenous leukemia epidemiolgy
- most common mpd, 20% of all leukemias, 40-50 y
- CML clinical
- - 20-40% are asymptomatic
- Fatigue, weight loss, night sweats
- WBC ~ 100K
- CML genetic pathogenesis
- BCR on chr 22 fuses w/ABL on chr9. BCR-ABL is a constitutively active kinase, 1) decreased adhesion of cells in bone marrow (loss of substrate-dependent growth inhibition), 2) increased proliferation through Ras, 3) inhibition of apoptosis.
- cml histology and genetics, chronic vs. accelerated phase
- Chronic Phase:
- BM – hypercellular, blasts <10%
- Peripheral – myeloblasts <2%
- Absolute basophilia
- BM/Peripheral – myeloblasts <20%
- Peripheral basophilia >20%
- Leukocytosis, splenomegaly
- more cytogenic abnormalities
- BM – blasts >20%
- 70% myeloid blast crisis - AML
- 30% lymphoid blast crisis - ALL
- Leukamoid Reaction vs. CML
- Leukemoid Reaction vs. CML
WBC: < 30K >30K
Toxic PMNs: Present Absent
Basophilia: Absent Present
Nucleus RBC: Absent Present
Platelets: Variable Increased
- Leukamoid Reaction vs. CML clinical presentation
- Splenomegaly Absent Present
Leukamoid Rx vs CML
Fever Present Absent
LAP Increased Normal
Karyotype Normal 9:22 + others
- Leukamoid Reaction vs. CML bone marrow appearance
- leukamoid rx vs cml marrow
Cellularity Hypercellular Hypercellular
M:E Ratio Increased Increased
Megakaryos Normal Abnormal
Blasts UP No Yes
- myelodysplastic syndrome epidemiology
- Exponential increase past 40
High progression to AML
History of chemo, radiation, toxins
- Myelodysplastic syndrome clinical presentation
- - Unexplained serious cytopenias, refractory to treatment
- myelodysplastic syndrome pathogenesis
- Acquired genetic abnormality of a plburipotent stem cell -> ineffective hematopoiesis.
- myelodysplastic syndrome cell types, prognosis
- Low grade – refractory anemia, normal blasts, +/- sideroblasts, 6 y.
High grade – refractory anemia w/ excess blasts, chemo/radioation history, multiple cytogenetic abnormalities, 6-8 mo.
- myelodysplastic syndrome histological appearance
- - Hypercellular marrow, cells with dysplastic morphology
- Peripheral cytopenias
1. Erythroid – dyssenchronous maturation of nucleus and cytoplasm, abnormal nuclear lobulation, multinucleated cells, ringed sideroblasts (iron granules in cytoplasmic periphery).
2. Granulocyte – bilobed neutrophils (Pelger-Huet cells), no cytoplasmic granules
3. Platelets – no granules, cells maybe huge (Giant platelets).
- myelodysplastic syndrome treatment
- supportive, BM transplant not for older pt's
- Polycythemia Vera epidemiology
- Polycythemia vera clinical
- - Hyperviscosity of blood (PCV >53%)
- Thrombotic episodes in mesenteric, portal, splenic veins
- GI bleeds
- Polycythemia vera pathogenesis
- Increased RBC production.
JAK2 kinase seems to be unregulated in many MPD, JAK2 phosphorylates GFRs, leading to proliferation.
- polycythemia vera lab diagnosis, polycythemic vs spent phase
- Polycythemic Phase:
- RBC heavy, Hb > 18.5 g/dL m, > 16.5 g/dL f.
- myeloid proliferation, thrombocytosis
- cytopenias, anemias, BM fibrosis, extra-medullary hematopoiesis, splenomegaly ~> AL low, increases if cyotoxic agents were used in the past.
- Chronic Idiopathic Myelofibrosis
- 1/100K 70 y
bone marrow failure 3-5 years
- chronic idiopathic myelofibrosis clinical features
- - 30% asymptomatic
- Fatigue, weight loss, fever, bleeding, gouty arthritis, renal stones.
- Chronic Idiopathic Myelofibrosis
blood smear and marrow
- - Mild anemia, mild leukocytosis, thrombocytosis
Smear: Nucleated RBCs, immature myeloid cells, teardrop RBCs
BM: hypercellular (granulocytic/megakaryocytic hyperplasia), osteosclerosis and fibrosis.
- Essential thrombocytopenia
women can presnt mid 30s
- essential thrombocythenia
- - Thrombocytosis and/or Hemorrhage
- essential thrombocythemia differential
- Must exclude: Infection, Neoplasm, Fe deficiency anemia, splenectomy. *Spleen sequesters platelets.
- essential thrombcythemia bone marrow appearance
- BM- hypercellular, enlarged, dysplastic megakaryocytes
- Multiple Myeloma epidemiology
- m=f 60s
- multiple myeloma clinical
- - Bone pain, ostelytic lesions
- Renal insufficiency
- Death from Infections, marrow/renal failure
- multiple myeloma pathogenesis
- Loss of chromosome 13.
*MGUS – in patients with monoclonal Ig in serum or urine, but no MM.
In BM there are no clumps, no lytic lesions, or depression of normal Ig, may get amyloidosis.
- Multiple Myeloma
histological appearance, lab dx
- BM- clumps of cells, monotypic Ig in the cytoplasm (little inclusions)
Plasma cells: eccentric nuclei, punched out nucleoli, basophilic cytoplasm.
Urine/Serum – bence jones/monoclonal Ig
- infectinos of esophagus
- Fungal – debilitated patients, Candida
Viral – leukemia/lymphoma patients, HSV, CMV
Bacterial – 2º site in lung infections
- esophagitis presentation
- - Dysphagia, pain, dyspepsia
- Bleeding, stricture, Barrett’s esophagus
- esophagitis pathogenesis, histo
- Malfunction of LES leads to acid reflux. Mucosa is injured by low pH. May lead to ulceration and erosion
Inflammation w/ eosinophils
- Barret's esophagus sx
- Dysphagia, pain, dyspepsia
- barret's esophagus pathogenesis
- Squamous mucosa replaced with metaplastic columnar epithelium -> dysplasia -> adenocarcinoma.
- Barret's esophagus tx
- regular screening/biopsy every 6 mo
- squamous cell carcinoma of esophagus epidemiology
- 4% of all cancer deaths in US, 4M:1F
achalasia, stricture, esophageal stricture
27% at 5 yrs
- esophageal squamous cell carcinoma sx
weight loss, anorexia
- squamous cell carcinoma of esophagous gross appearance
- 3 types
fungating exophytic mass
ulcerated, eroding mass (nearby vessels!)
- squamous cell carcinoma histo appearance
- well--> poorly differentiated
(keratinization and intracellular bridges)
- esophageal adenocarcinoma epidemiology
- now 50%, Barrett’s
80% lower 1/3, 50% extend into the stomach
70% flat/ulcerated, 30% fungating, W>AF
- esophageal adenocarcinoma sx
- - Dysphagia
- Weight Loss, anorexia
- esophageal adenocarcinoma pathogenesis
- Long standing Barrett’s esophagus with high grade dysplasia, cells resemble intestines, but can look like cells found anywhere along the GI tract.
- esophageal adenocarcinoma histo/labs
- Cancers look like glands, tubules or signet rings. 75% node mets @ diagnosis,
- Acute Gastritis epidemiology
- Common, mild to severe (hemorrhage), 30% of upper GI bleeds, aspirin, nsaids, etoh, smoke, chemo, staph food poisoning, uremia, shock, helicobacter pylori
- Acute Gastritis clinical
- - Pain
- Ulceration/Erosion of mucosa
- Upper GI bleeds (hematemesis)
- Lower GI bleeds (melena)
- Acute Gastritis pathogenesis
- Direct injury to mucous cells (aspirin) breakdown of the mucous barrier, blood shunting mucosal damage.
- Acute Gastritis histo/labs
- Gross: edema, petechiae or frank hemorrhage
Micro: acute inflammation w/ PMNs, sometimes mucosa sloughs off.
- Chronic Gastritis epidemiology
- Mild to severe, chronic gastritis in 50% of older patients,
H. pylori, immune (pernicious anemia), billiary reflux (post surg), smoke, etoh, radiation, uremia.
- Chronic Gastritis clinical
- - Chronic active gastritis – H. pylori + lots of PMNs
- Chronic superficial gastritis – H. pylori + lymphocytes/plasma cells
- Chronic atrophic gastritis – atrophy of gastric glands
- Autoimmune – fundus
- H. pylori – antrum
- Hypochloridia (due to loss of parietal cells ~ autoimmune)
- Gastric Carcinoma
- Chronic Gastritis pathogenesis
- H. pylori – G-, spiral rod, acute/chronic gastritis + carcinoma. Produces urease damages mucosal barrier epithelial injury by H ions + protease/phospholipase injury + myeolperoxidase from PMNs, thrombotic occlusion of vessles.
Autoimmune - <10%, auto-abs vs. parietal cells and intrinsic factor gland destruction, mucosal atrophy ~> pernicious anemia.
- Chronic Gastritis histo/labs
- Gross: mucosa is swollen or flat/thin, shiny.
Micro: lymphocytic & plasma cell infiltrate, lymphoid aggs in mucosa, some PMNs in gastric glands.
- Chronic Peptic Ulcer Disease epidemiology
- Chronic solitary ulcers, decreased, 4mil in US, M>F, middle age
Psychological, env – aspirin, steroids, nsaids, etoh, coffee, cola, smoke, cirrhosis, copd, CRF, hypercalcemia, h. pylori toxins, changes in gastric secretions.
- Chronic Peptic Ulcer Disease clinical
- - Bleeding – most common cause of upper GI bleeds (minor massive)
- Perforation – 5%, high mortality
- Obstruction – in pyloric or duodenal ulcers
- Pain – recurrent
- Cancer – 10% of gastric ulcers are malignant from the start, but chances of cancerous progression from normal are probably 0%.
- Chronic Peptic Ulcer Disease pathogenesis
- Associated with chronic gastritis and H.pylori.
Duodenum – ant/post wall 1st seg, 2nd seg
Stomach – antrum, lesser curvature.
Meckels, lower esophagus, anastomatotic ulcers.
Duodenal Ulcers: hypersecretion of acid & pepsin (~parietal # ↑, or hypersensitivity of parietal cells), rapid gastric emptying.
Gastric Ulcers: NOT associated with increased acidity, mucosal damage via billiary reflux, H ions implicated, + shunting of mucosal blood flow.
- Chronic Peptic Ulcer Disease gross appearance
- Gross: punched out/deep, solitary, sharp edges VS. Acute gastric ulcers - which are multiple, not deep and not scarred.
- Acute Gastric Ulcers epidemiology
- Severe illness & stress – patients in ICU, up to 10%.
Brain – Cushing’s
Burns – Curling’s
Shock & Sepsis
Aspirin & NSAIDs
- Acute Gastric Ulcers
- - Bleeding (minimal to massive)
- Pain (masked)
- Acute gastric ulcers pathogenesis
- In Some – acute ulcers from acute gastritis, with erosions and ulcerations (mucosal blood shunting).
- Acute gastric ulcers gross and micro appearance
- Gross: superficial, small, multiple lesions with ragged edges, occur anywhere in the stomach.
Micro: acute inflammation, fibrinoid necrosis, granulation tissue, no scarring.
- Hypertrophic Gastropathy appearance
- enlargement of rugal folds of gastric mucosa
- Menetrier’s disease
- expansion of foveolar epithelium, rare, men 30-50, excess mucous production, hypchloridia (low parietal cells), loss of protein because of abnormal mucosa (peripheral edema)
- Zollinger-Ellison syndrome
- gastrinoma excess gastrin parietal cells hyperplasia enlarged folds, peptic ulcers.
- Benign Gastric Tumors
- Less common than colonic polyps, incidental, in chronic gastritis setting. Polyps are made of elongated and hyperplastic foveolar epithelium.
Adenomas – rare, <10% of polyps, sessile or pedunculated, antrum. Large may progress to adenocarcinoma.
- Gastric Carcinoma epidemiology
- Japan >> US
Food preservation, diet, nitrosamines.
H. pylori, Blood A, hypchloridia.
Early – 95% @ 5 y
Adv – 10% @ 5 y
- Gastric Carcinoma
linitis plastica vs intestinal vs diffuse
- Linitis plastica – flat, spreading lesion, walls are thick, hard to diagnose.
Intestinal ~ colon adenocarcinoma, glandular formations, H. pylori, down in western world.
Diffuse – cells from native gastric glands, no metaplasia.
- gastric carcinoma parts of stomach %s
- Pylorus, antrum – 55%
Cardia – 25%
Rest – 20%
- Gastric Mesenchymal tumors pathogenesis
- Spindle cell neoplasms, from the wall of the somach (Interstital cells of Cajal – pacemaker cells). Used to be called leiomyomas and leiomyosarcomas -> gastrointestinal stromal tumors.
- Causes of pancreatic insufficiency
- cystic fibrosis, pancreatitis –> loss of pancreatic enzymes
- Whipple’s disease
- hypersensitivity to gluten – gliadin, component of gluten, in grains causes immunologic flattening of villi, increased risk for T cell lymphoma and adenocarcinoma of small intestine
- congenital – dilated lacteals/lymphatics -> obstruction -> ineffective transport
- Drugs which cause malabsorption
- cholestyramine, colchicines, para-aminosalicylic acid, cathartics, neomycin
- Dysentery sx, epi, causes
- Low volume, painful diarrhea, 12k/day deaths, 50% under 5. Rotavirus, Norwalk, Enterotoxigenic E. coli.
- Bacterial Enterocolitis, which bugs:
ingestion of toxin?
ingestion of bacteria?
ingestion of enterinvasive bacteria?
- Ingestion of toxin – S aureus, Vibrios (cholera), C. perfringens
Ingestion of bacteria – E.coli, Campylobacter
Ingestion of enterinvasive bacteria – Salmonella, Shigella, Campylobacter, Y. pestis.
- GI congenital malrotation
- disordered counterclockwise rotation (around SMA), 1 in 6K, present with obstruction.
- GI congenital duplications
- small/large bowel, present with mass, pain (obstruction, intussusception, perforation).
- failure of development of anterior abdominal wall, gut covered by peritoneal membrane.
- failure of development of anterior abdominal wall, gut NOT covered by peritoneal membrane.
- Atresia (GI)
- complete obstruction, most common in duodenum, least in colon. Mesenteric arterial occlusion in utero.
- incomplete obstruction of vitelline duct, located within some distance of ileocecal valve. Ectopic gastric or pancreatic tissue might be present -> ulceration of small intestines. Bleeding, intussusceptions, perforation.
- Congenital aganglionic megacolon (Hirschsprung)
- (Hirschsprung) – aberrant migration of neural crest cells, aganglionic colon cannot produce peristaltic movements, and so everything backs up, normal colon dialates, 4M:1F.
- intestinal adenocarcinoma common sites, types, sx
- Ampulla of Vater
Napkin ring or polypoid
- Fatigue, hemorrhage
- Carcinoid, sites, sx
- 60 yo, appendix, ileum
- Flushing, cyanosis
- Diarrhea, cramping
- RH valvular lesions (T stenosis)
- Edema & Arthirits
- carcinoid pathogenesis, histo appearance
- Enterochromaffin cells produce increased tryptophan metabolites --> serotonin, bradykinin, histamine, prostaglandins. Cells are in nests, of glandular appearance.
- carcinoid lab finding
- 5-HIAA – serotonin metabolite
- pseudomembranous colitis sx
- - Acute or Chronic diarrhea w/o history of bowel disease
- pseudomembranous colitis pathogenesis
- Treated with broad-spectrum Abs, destroying the normal flora of the intestines, allowing C. dificile to overgrow and secrete toxins A/B damage mucosa fibropurulent exudates (adheres to the mucosa)
- pseudomembranous colitis micro and gross
- Gross: yellow exudates on an inflamed mucosa.
Micro: pseudomembranes adherent to the surface of mucosa, PMNs in lamina propria, thrombi in vessels
- pseudomembranous colitis tx
- Treat with metronitazole
- Crohn’s Disease epid
- 3/100K, F>M, Jews, 15-20 & 55-65 y, 40% family history. abnormal immune activation of T cells. SB – 40%, SB LB – 30%, LB – 30%.
- Crohn's clinical comp, presentation
- Localized – fistulas (10-15%), hemorrhage, strictures, risk of malignancy (2%)
Systemic – hepatic inflammation, arthritis, uveitis, erythema nodosum, nutritional deficiencies, anorexia, malabsorption.
- Croh's gross appearance
- Gross: skip lesions, thrush-like ulcers, thickened inflexible small bowel wall, narrowed lumen, “creeping fat”, wall of colon not thickened.
- Crohn's micro appearance
- Micro: transmural inflammation, non-caseating granulomas, dilated lymphatics, lymphoid aggregates, thickened nerve bundles, normal surface mucus production.
- Ulcerative Colitis epid
- Only colon, recurrent ulcero-inflammatory disorder, backwash ileitis, 6/100K, same etiology ?!
- Ulcerative colitis clinical complications, sx
- Localized – toxic megacolon -> perforation w/ 30% mortality, hemorrhage, stricture, carcinoma risks increase if UC is chronic, w/ multiple recurrences and is extensive. Systemic – hepatitis, hemolytic anemia, ankylosing spond, arthritis, uveitis, embolism,
EN & PG
- ulcerative colitis gross appearance
- Gross: begin in the rectum, backwash ileitis, inflammatory pseudopolyps, mild bowel thickening.
- ulcerative colitis micro appearance
- Micro: crypt abscesses -> ulcerations, mucosa only, never transmural (toxic megacolon – ulceration destroys the muscle layer, and no peristalsis occurs). Walls might be fibrotic, pseudopolyps, higher carcinoma risk, decreased mucus production
- transmural infarction of intestines
- necrosis of all layers, occlusion of major artery
causesd by atherosclerosis, arteritis, dissecting aneurysm, hypercoag, surgical, hyopperfusion (shock, hypotension, HF) – 75% mortality.
- Angiodysplasia of GI
- malformation of submucosal and mucosal blood vessels (right colon, or cecum), 20% of lower GI bleeds, wall tension.
- Hemorrhoids pathogenesis
- maybe due to distal displacement of the anal cushions from:
constipation, pregnancy, portal hypertension.
- Diverticular Disease epid
- 50% in ppl >60 yo, uncommon in east, diet
- diverticulosis clinical comp
- - Inflammation – 20%, abscess formation
- Fistula – abscess extending into an adjacent organ.
- Obstruction and bleeding
- diverticular disease gross appearance
- Gross: herniations of mucosa through the muscularis layer, large and small bowel (mesenteric side of sigmoid colon).
- Hyperplastic Polyps pathology, gross app
- Increased cell proliferation in lower 3rd of the crypt, normal differentiation. Most common in rectosigmoid colon. No risk of malignancy.
Gross: <5 mm, saw-tooth appearance.
- juvenile polyps epid
- Children 1-7 yo
Congenital, sporadic or juvenile polyposis syndrome (aut dom).
- juvenile polyps classification, complications
- Type of hamartamatous polyps. If part of Juvenile Polyposis Syndrome can be associated with carcinoma, otheriwise no increased risk of malignancy. Most common in rectum
- juvenile polyps gross & micro
- Gross: <3cm
Micro: acute inflammation of lamina propria, cystic glandular spaces.
- Petz-Jeghers Polyps epid
- Aut. Dom, higher chance of cancer else where in the body
- Petz-Jeghers Polyps clinical
- Melanin pigmentation of lips, buccal mucosa, webs of fingers/toes, hamartomatous polyps/
- Petz-Jeghers Polyps micro and gross app
- Cells are normally differentiated, arborizing network of smooth muscle and connective tissue in the lamina propria
Gross: 2-3 cm,
- Cowden Syndrome epid, what is?
- Aut Dom, thyroid and breast cancer up
Hamartomatous polyps in GI, facial trichilemal tumors, acral keratoses, oral papilomas
- Cronkite – Canada Synd.
- Hamartomatous polyps in GI, nail atrophy, skin pigmentation and alopecia.
- Inflammatory Polyps
- Not true polyps, occur in Ulcerative Colitis.
- Tubular Adenoma epid
- 75% of polyps, 60yo
- Tubular Adenoma
- Abnormal cellular proliferation, mutation of APC gene is postulated. All of the cells in the crypt can proliferate. Atypical cytology, mild or high grade.
Pedunculated or sessile, most commonly in the colon, also stomach and SB. Test-tube shaped glands, cells are crowded with pseudostratified nuclei.
- Villous Adenomas
- Usually sessile, can be very large (<10 cm), cells arranged in papillary fronds. Cytological atypia.
Water, electrolyte loss, bleeding.
Less common, rectum
- Tubulovillous Adenoma
- 20-50% of polyp has villous features.
Increased risk of developing cancer.
- Serrated Adenomas
- <1%, right side of colon
Sessile or pedunculated, serrated glands lining crypts in a pattern similar to the hyperplastic polyp. Glands are stratified and dysplastic. Goblet cells look immature, upper zone mitosis is apparent.
- Heredofamilial Polyps
- Familial Polposis 1/16K, Aut Dom.
Polyps may be numerous (>100), mucosa looks fuzzy. Inevitable cancer progression.
- Gardners Syn.
- Aut Dom.
Have soft tissue tumors (fibromatosis, osteomas, lipomas) + adenomatous polyps. Similar to above in morph and prog.
- Turcots Syn.
- Aut. Recessive
Have brain tumors (gliomas) + adenomatous polyps
- Colon Adenocarcinoma EPID
- 2nd death US, geography ~ diet.
Cholesterol + low fiber increase risks.
Aspirin, anti-oxid, vitA,C, selenium, zinc, calcium decrease risk.
- Colon Adenocarcinoma left vs right
- Left side (napkin ring) > Right side (fungating).
- Carcinoid Tumors
- Rare, 60 y (22-80s range). 90% in GI, M=F.
Neuroendocrine (enterochromaffin) cells. Secretion of various substances.
Monotnous cells, few mitotic numbers. IC, silver, Abs to chromogrannin.
- Appendicitis problemmes
- - Perforation
- appendicitis pathology
- Obstruction by fecaliths ischemia bacterial overgrowth invasion of mucosa bloodstream.
Hemorrhagic or purulent, acute inflammation of the lumen, extending into muscularis, PMNS in muscularis.
- Bladder Carcinoma epid
- 95% - epithelial (transitional cell)
M3:F1, 50-80 yo
Smoking, chemicals, cytoxan, Schistosoma haematobium, chronic infections.
Del chr9, p16, p53. 70% confined to bladder at diagnosis.
- Bladder Carcinoma clinical
- - Hematuria
- ‘Field Effect
- Bladder papilloma vs carcinoma
- Papilloma – benign, papillary arch, normal urothelium, rare, younger patients, do not progress.
Carcinoma – low grade ~ papillary, high grade ~ nodular, ulcerated, flat. Cells resemble urothelium.
- Bladder carcinoma grade and stage
- Grade based on polarity, crowding/overlapping, cytological atypia, pleomorphism, mitosis.
Stage based on depth of invasion (muscularis propria) +/- mets
- bladder carcinoma prog (non ivasive vs LP invasion), tx
- Recurrence and progression (based on stage/grade) common. Non-invasive – follow
LP invasion - Alkylating agents, attenuated mycobacterium BCG (necrotizing granuloma response),
Deep LP invasion – cystectomy
Metastatic - chemo
- Mesenchymal Bladder Tumors peds vs adults; tx
- Peds – Rhabdomyosarcoma; embryonal or botryoid subtypes ~ small or oval spindle cells, with skeletal muscle differentiation (desmin immuno-staining)
Adults - Leiomyoscaroma
tx w/ chemo
- Seminoma epid; risk factors
- Most common GCT
30s, never infants
50% of GCT
Chr12 abnormalities, Cryptorchidism.
- seminoma clinical
- - Painless mass/enlargement
- Exam, US, markers
- seminoma gross
- Gross: lobulated, circumscribed, gray-white, w/o necrosis/hemorrhage, replacing most/all of the testes (not penetrating tunica albuginea).
- seminoma micro
- Micro: cells in alveolar/tubular patterns push atrophic tubules aside, basal nuclei and atypical cytoplasm, situated among sheets of undifferentiated cells. Cell borders are poorly defined, and are of varying sizes and shapes. Mitotic figures may be frequent.
- seminoma labs
- +/-- HCG, +/-- AFP
- Choriocarcinoma clinical
- - May present with symptoms due to metastasis (shortness of breath).
Common in NSGCT
- choriocarcinoma of the balls gross app
- Gross: small palpable nodules that don’t cause enlargement. Hemorrhagic and necrotic areas. Grow faster than blood supply -> fibrous scar + mets.
- choriocarcinoma micro
- Micro: Syncytiotrophoblastic cell – large, multinucleate, vacuolated pink cytoplasm. Cytotrophoblastic cell – round cells with prominent nucleoli
- choriocarcinoma of the balls labs
- + HCG
- Teratoma teratoma of the balls epid
- Any age, pure forms common in infants, rare in adults, common in NSGCT
- teratoma of the balls gross appearance
- Gross: large, heterogeneous appearance, hemorrhage and necrosis indicate presence of embryonic carcinoma & choriocarcinoma.
- teratoma of the balls micro
mature vs immature
- Micro: mature (well differentiated elements) vs. immature (small blue cells, may become malignant SCC, adenocarcinoma, sarcoma). Same treatment.
- ITGCN (Intratubular germ cell neoplasia)
- Seen in association with all testicular GCT in adults, presumed to be the precursor lesion. Reduced/absent spermatogenesis, in tubules there are few layers of atypical cells with large nuclei, prominent nucleoli, clear cytoplasm. Marker: + Alkaline Phosphatase.
- Benign Prostatic Hyperplasia epid
- Histologic -40s
Age, androgen metabolism
DRE – normal
Not a precursor to cancer.
- Benign Prostatic Hyperplasia clinical
- - Obstruction, hesitancy, intermittency, dribbling.
- Bladder hypertrophy -> decompensates -> stasis, frequency, nocturia, UTI, bladder stones, hydronephrosis, renal insufficiency.
- Benign Prostatic Hyperplasia pathogenesis
- 5-α-reductase converts testosterone to DHT, this enzyme is increased in ppl with BPH. Serum testosterone decreases. Estrogen upregulates receptors for DHT in the porstate more androgen receptors in prostate, more sensitive to DHT from 5-α-R. Occurs in the periurethral transition zone surrounding prostatic urethra. Increased α-adrenergic activity more smooth muscle contraction around urethra
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