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334 Cards in this Set

  • Front
  • Back
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
Indolent, relapse
5-8 years survival
50% -> aggressive large cell lymphomas
Follicular B cell lymphoma sx
painless adenopathy
B symptoms
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
High mitosis
Diffuse Large B cell surface antigens
Surface Ig
CD10 +/-
B cell Lymphoma
Most aggressive
Children, immunodeficient

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
CD5-, CD10+
extranodal MALT B cell lymphoma; epidemiology,
adults in their 60s
Extranodal MALT B cell lymphoma clinical appearance
incidental finding
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-

CD19+; CD20+
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

resp/cardiac compromise

pleural/pericard effusions
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

-CD4 subset
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

B symptoms

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

young patients
Nodular sclerosing hodgkins 'classic' patient
young females
nodular sclerosing hodgkins clinical presentation
Cervical lymphadenopathy

Mediastinal mass

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

CD15+; CD30+
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

CD15+; CD30+
Lymphocyte rich hodgkins histological appearance
small lymphocytes
Lymphocyte and histiocyte morphology RS cells (popcorn)
Lymphocyte depleted hodgkins epidemiology
adult males
*most aggressive
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
young males
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
(popcorn cells)
lymphocyte and histiocyte RS cell antigens
CD45+; CD20+ (b cell marker)

CD15-; CD30-
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
auer rods
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

Acute lymphoblastic leukemia epidemiology
85% of childhood leukemias

15% adults
mostly b cells
acute lymphoblastic leukemia clinical presentation
mediastinal mass in a young male

hepatosplenomegaly, lymphadenopathy

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

Lymphoblastic Lymphoma

Most common in western world.
~65 y.o.
Indolent, 7 y
Chronic Lymphocytic Leukemia

Lymphoblastic Lymphoma

Clinical presentation
- Often asymptomatic
- Fatigue
- Anemia, infections
- Hepatosplenomegaly, lymphadenopathy
- Hypo-gammaglobulinemia
- WBC 10K – 300K
Chronic Lymphocytic Leukemia

Lymphoblastic Lymphoma

biochemical pathogenesis
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

Lymphoblastic Lymphoma

histological appearance
- Lymphocytosis (>10K), anemia, thrombocytopenia.
- Hypogammaglobulinemia
- 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

Lymphoblastic Lymphoma

laboratory diagnosis
- 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
- Splenomegaly
- 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
- 9:22
Accelerated Phase:
- BM/Peripheral – myeloblasts <20%
- Peripheral basophilia >20%
- Leukocytosis, splenomegaly
- more cytogenic abnormalities
Blast Phase:
- BM – blasts >20%
- 70% myeloid blast crisis - AML
- 30% lymphoid blast crisis - ALL
Leukamoid Reaction vs. CML
WBC count
Toxic PMNs
Nucleus RBC
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
M:E Ratio
Blasts UP
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
- Symptomatic/incidental
myelodysplastic syndrome pathogenesis
Acquired genetic abnormality of a plburipotent stem cell -> ineffective hematopoiesis.

Abnromal/normal cytogenetics.
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
Spent Phase:
- 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.
- Splenomegaly
- Hepatomegaly
Chronic Idiopathic Myelofibrosis

histo appearance
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
- Splenomegaly
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
- Hypercalcemia
- Renal insufficiency
- Amyloidosis
- 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
EtOH, smoking
achalasia, stricture, esophageal stricture
not genetic
27% at 5 yrs
esophageal squamous cell carcinoma sx
weight loss, anorexia
squamous cell carcinoma of esophagous gross appearance
3 types
fungating exophytic mass
flat, diffuse
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
- Pain
- Weight Loss, anorexia
- Fatigure
- Ulceration/bleeding
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
- Bleeding
- 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)
- Ulceration
- 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

- Obstruction
- Jaundice
- Fatigue, hemorrhage
Carcinoid, sites, sx
60 yo, appendix, ileum

- Flushing, cyanosis
- Diarrhea, cramping
- RH valvular lesions (T stenosis)
- Wheezing
- 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,
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.
what is?
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
Rectosigmoid colon.
Tubular Adenoma

pathology, appearance
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
- Abscesses
- Pyelophlebitis
- Septicemia
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).

Highly malignant
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
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.
Hemorrhagic infarction.
- 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
benign prostatic hyperplasia gross appearance
Gross: large nodules in transition zone, pink-tan or gray, median lobe prominence.
benign prostatic hyperplasia micro appearance
Micro: mixture of glands and fibromuscular stroma, hyperplasia. Glands are elongated, with 2 cell layers (secretory & basal). No cytologic atypia, mild lymphoid infiltrate.
benign prostatic hyperplasia tx
TURP, 5-α-R inhibitor (Proscar), α-blockers.
Prostate Cancer epid
200K-300K /y, 40K deaths, latent vs. clinical, >40, 80s highest, US>>East, W<AF, testosterone, oncogenes, GFs. Alkaline phosphatase elevated in metastatic tumors.
Prostate Cancer clinical
- Obstruction, hematuria in patients with progressed
- Mets to pelvic lymph nodes, bone ~ osteoblastic mets (bone formation stimulated by the tumor)
prostate cancer PIN, DRE
PIN (~10 years) -> lesion in the peripheral zone (60-80%), gleason score based on architechture and not cytological features (2 scores, given as sum).
DRE (abnormal nodules in posterior lobes), TRUS biopsy (sextant approach), PSA (Serine protease; normal ~ 0-4 ng/mL, rise -> rise in cancer %, also important to follow post-treatment).
Prostate Cancer gross, micro
Gross: firm, tan-gray

Micro: small crowded or infiltrating glands invading the stroma, large nuclei/nucleoli, loss of basal layer (loss of keratin staining)
prostate cancer tx
T1, T2 – surgery. Radiotherapy if extension beyond the gland. Hormones for mets (LHRH analogues, inhibitors of androgen synthesis, androgen blockers).
Acute Salpingitis epid
60% gonococcus
40% Chlamydia + enteric
Component of PID
Acute Salpingitis clinical
- Pelvic pain
- Adnexal tenderness
- Fever
- Vaginal discharge
salpingitis pathogenesis
Originates in Bartholin, vestibular, periurethral glands, involves the cervix -> towards uterus -> tubo-ovarian abscesses, peritonitis, sepsis.
Non-STD~puerperal fever (staph, strep, c. perfringens)
acute salpingitis findings
Lumenal fibrosis, infertility, hydrosalpinx (cysts), peritoneal obstruction
ectopic pregnancy risk factors
PID w/ chronic salpingitis, endometriosis,
ectopic pregnancy pathogenesis, tx
Placental tissues in the wall -> dilation -> hemorrhage into the lumen -> placental tissue invades through the wall -> rupture -> hemorrhage into the peritoneum -> shock

Methotrexate – induces spontaneous involution of tubal gestations.
Paratubal Cysts
Common, asymptomatic, insignificant

Small, unilocular, clear fluid, lined by transitional epithelium.
Hydatid cyst of Margagni – large cyst of mullerian duct origin, at the fimbriated end of the tube.
Adenomatoid Tumor

Mesothelial origin in the subserosal region of the tube.
Fallopian Adenocarcinoma
Rare, more often it’s a secondary site (ovaries or endometrium)

Serous or endometrioid differentiation,
Ovarian Inflammation

sx, pathogen
Rare, hydrosalpinx can be a complication due to blockage

Tubo-ovarian abscess ~ PID (Gonorrhea, Chlamydia)
Infectious Oophoritis ~ mumps, CMV, actinomyces, fungus, TB
Autoimmune Oophoritis
Endometriosis, epid, locations
30s-40s, Ovaries, uterine ligaments, rectovaginal septum, 10% of all women
endometriosis sx
- Infertility
- Pain (dysmenorrhea)
- Bleeding
Endometriosis pathogenesis
1. Retrograde menses through fallopian tubes  tissue into the peritoneum.
2. Metaplasia  endometrial tissue
3. Lymphovascular travel (found in lymph nodes & lungs
endometriosis pathology, gross and micro
Gross: responsive to normal cycle (bleed  chocolate cysts), adhesions.
Micro: Endometrial glands, endometrial stroma, hemosiderin pigment (2 of 3)
Follicular Cysts
Young women

Single enlarged corpus luteum +/- hemorrhage, yellow lining of granulosa cells.
Polycystic Ovary
Disease epid
3-6% of rep. age women. Endometrial hyperplasia/carcinoma from unopposed estrogen production
polycystic ovary disease sx
- Oligomenorrhea
- Persistent anovulation
- Obesity (insulin resistance, hyperprolactinemia), hirsutism, virilism.
Polycystic Ovary Disease pathology
Continuous pre-ovulatory situation where LH and estrogen are at high levels. LH surge never occurs to inhibit estrogen and follicle never ruptures  anovulation.
Multiple follicle cysts  bilateral enlargement. Coretex is fibrosed, follicular theca cell hyperplasia, absence of corpora lutea (no progesterone).
Ovarian Tumors epid
80% benign, younger
Malignant – 50s-60s
Age, nulliparity, BRCA1, 2, gonadal dysgenensis
ovarian tumors sx
- Early – mild symptoms
- Abdominal pain, increasing girth, ascites, urinary/GI disturbances, vaginal bleeding, hormones (rare).
three types ovarian tumors
- Surface epitheliam tumors
- Sex cord stromal tumors
- Germ cell tumors
Surface Epithelium Tumors epid
65-70% of all ovarian tumors, 90% of malignant tumors, >20 yo, Mullerian epithelium -> Fall. Tube epithelium, endometrial, endocervical epithelium.
Malignant – penetrate ovarian capsule, grow on peritoneal surface.
Malignant cells in Ascites. Mets -> lungs, pleura, liver.
CA-125 up in 80%, surgery with chemo.
ovarian surface epithelium serous tumour

epid, benign, malignant
Serous – most common, majority benign, bilateral, assoc. with endosalpingosis and endometriosis. Benign – unilocular, clear fluid, smooth lining (i.e. cystadenomas). Malignant – papillary and solid areas, stromal invasion, necrosis (i.e. cystdenocarcinoma). Borderline – epithelial growth, papillations, crowding, infolding, NO stromal invasion. Malignant > benign (resembles fallopian tube epithelium).
mucinous ovarian surface epithelium tumor
Mucinous – majority benign, unilateral, multiloculated appearance, with viscous fluid, tall columnar mucin-producing cells. Benign (resembles endocervical epithelium) > malignant.
a) Endocervical – papillary architecture, bilaterality, endometriosis & endosalpingosis.
b) Gastrointestinal – resemble bowl lining, assoc. with pseudomyxoma peritonei, ~ 2ndary involvement from GI source.
endometroid ovarian surface epithelium tumor
Endometrioid – majority malignant, bilateral, assoc. with endometriosis. Adenofibromatous architecture, solid > cystic, 15-30% assoc. synchronous endometrial adenocarcinoma.
Clear cell ovarian surface epithelium tumor
Clear Cell – subset of endometrioid, assoc. with endometriosis, majority malignant & highly aggressive.
ovarian surface epithelium tumors: transitional
Transitional (Brenner) – majority benign, adenofibromatous architecture, assoc. with mucinous cystadenomas.
Sex-Cord Stromal Tumors epid
Least common 5-10% all ages, often benign. Arise from stromal cells (fibrblasts, SMCs) +/- sex-cord cells (granulosa, theca, sertoli, leydig).
Can produce hormones
granulosa theca sex cord stromal tumors. pathology
Granulosa-Theca – post menopausal women, mixture of both cell types, unilateral, cystic/hemorrhagic, yellow. Granulosa cells have oval nuclei with grooves, form eosinophilic grand-like structures – Call-Exner bodies. Can produce estrogen  precocious puberty in girls. Assoc. with endometrial hyperplasia, breast fibrocystic changes, endometrial carcinoma. Potentially malignant, late recurrence
Fibrothecoma and fibroma sex cord stromal tumors
Fibrothecoma & fibroma – benign, variable theca:fibroblasts. Estrogenic if theca component is large. Grossly solid white, areas of yellow (theca). Assoc. with ascites and right pleural effusion (Meig’s Syndrome), common in patients with Basal-Cell Nevus Syndrome. If malignant  fibrosarcoma.
sertoli leidig sex cord stromal tumors
Sertoli-Leidig – rare, mixture, masculinization through testosterone production.
Germ Cell Tumors epidemiology
2nd most common, bilateral 10-15%, Dysgerminoma (=seminoma), occur in pure form, most common form is mature teratoma.
Teratoma – cystic, ectodermal derivatives (skin elements). Characteristic mass with skin, hair, teeth, bone = Dermoid cyst. If pure a) thyroid elements (struma ovarii), b) neuroendocrine cells (carcinoid)
Dysgerminoma – young F, unilateral, fleshy, nodular, +/- necrosis/hemorrhage, sheets of cells, scattered lymphocytes.
Metastatic ovarian Tumors epid, primary loc's, types
Bilateral, primary sites are often mullerian – endometrium, contralateral ovary, fallopian tube. Extramullerian – breast, GI, biliary tract, pancreas.

Krunkenberg tumor – bilateral met tumor to the ovaries made of signet ring cells from GI.
Anovulatory Cycle causes
Most common cause of Dysfunctional Uterine Bleeding, menarche and menopause
Anovulatory cycle clinical
- Menorrhagia
- Metorrhagia
- Menometorrhagia
- Infertility
pathogenesis of anovulatory cycle
Related to endocrine disorders (thyroid, adrenal, pituitary), ovarian lesions (tumors, PCOD), obesity, malnutrition, chronic systemic illness. Without ovulation there is no corpus luteum development, thus no progesterone and the effect of estrogen during pre-ovulatory phase is unopposed. Abnormal proliferative pattern develops.
Luteal Phase Defect
- Menorrhagia
- Metorrhagia
- Menometorrhagia
- Infertility
luteal phase defect pathology
Deficient corupus luteum function -> low progesterone output. Biopsy shows dysynchronous development of endometrium with what is expected.
Endometritis, sx
- Abnormal bleeding
- Pain
- Discharge
- Infertility
Endometritis acute vs chromic
Acute – uncommon, due to puerperal fever and is polymicrobial, may -> PID.

Chronic – assoc. with PID, can affect fallopian tubes and ovaries. Chlamydia > retained tissues from gestation > IUD > TB/fungal disease…-> severe chronic infection.
Endometritis histo appearance
Abnormal prolif phase, undatable pattern, reactive stroma with spindled cells. Lymphocytes, MCs, PLASMA CELLS.
uterine polyps epid
40s-70s, posterior wall of the uterus. Rarely  adenocarcinoma
uterine polyps sx
- Asymptomatic
- Abnormal bleeding
uterine polyps pathology
Non-neoplastic overgrowths of endometrial lining, single/multiple

Fibrous stroma with prominent vasculature, glands maybe functioning or hyperplastic & cystically dilated. Respond to estrogen (Tamoxifen).
endometrial Adenomyosis sx
- Asymptomatic
- Pain
- Abnormal bleeding (before/after periods)

uterine adenomyosis pathology
Perimenopausal, form of endometriosis

Uterus enlarged, myometrium thickened, cystic spaces +/- hemorrhage.
Endometrial glands and stroma found within myometrium, 2-3 mm away from endometrial basalis.
Hormonaly responsive, cycle with normal endometrium.
Endometrial Hyperplasia sx
- Abnormal uterine bleeding
endometrial hyperplasia epid
Too many glands, unopposed estrogen, perimenopausal (freq. anovulatory cycles), obesity, PCOD, granulosa cell tumors, tamoxifen therapy - ↑ estrogen
Endometrial Hyperplasia histo appearance
Simple/Complex architecture +/- Cytological Atypia.
Simple – glands with tubular config, similar to normal endometrium.
Complex – variably sized glands, crowding, irregular, infolded profiles.
Cytological atypia – nuclear stratification, N:C ratio up, hyperchromasia, mitotic figures – 23% -> endometrioid adenocarcinoma
Stromal invasion distinguishes between atypical hyperplasia and cancer.

Hormonal therapy +/- hysterectomy.
Endometrial Adenocarcinoma epid
Most common cancer of female RT, peri/postmenopausal, obesity, diabetes, HTN, infertility. Smokers decreased%. Mort/Morb – RF, infx, hemorrhages.
Endometrial adenocarcinoma sx
- Abnormal/postmenstrual

Prolonged, unopposed estrogen stimulation.
Stage and grade important. Majority are quite indolent, discovered early, with good prognosis.
endometrial carcinoma, name the types
endometriod and serous (more common more aggressive. looks like ovarian serous tumor)
Endometrioid endometrial adenocarcinoma
Endometrioid – most common, due to unopposed estrogen-stimulated hyperplasia (obesity, PCOD, anovulation, hormonally active tumors, tamoxifen therapy).
Gross: localized polypoid masses or diffuse replacing the endometrial surface.
Micro: stratified columnar malignant cells, invading the stroma and myometrium. Squamous Metaplasia found within the glands. Spread by direct invasion, and eventually to pelvic/iliac nodes and to lungs, liver, bones
serous endometrial adenocarcinoma
Serous – less common, elderly patients, NOT assoc. with estrogen or hyperplasia. P53 mutations in all tumors, look like malignant ovarian serous tumors. High grade, very aggressive. Spread on the peritoneal surfaces
Malignant Mixed Mullerian Tumor, sx, epid
- Postmenopausal bleeding

Very aggressive
Elderly patients
Malignant Mixed Mullerian Tumor pathogenesis
Malignant epithelial (HG endometrioid or serous adenocarcinoma) and mesenchymal (uterine SM or skeletal muscle, bone or cartilage) elements  single cell of origin.
Malignant Mixed Mullerian Tumor appearance
Large polypoid mass in uterine fundus may protrude through cervical os.
Endometrial Stromal Tumors, epid
Benign or malignant
Endometrial Stromal Tumors pathology
Stromal nodule – well circumscribed proliferation of stromal cells ~ leiomyoma, insignificant.
Endometrial stromal sarcoma – malignant, infiltrates myometrium diffusely & extensively, metastatic potential.
Leiomyoma epid
Benign, 30% of all menstruating f > 30
leiomyoma sx
- Pelvic mass
- Vaginal bleeding
- Pelvic pain
Types leiomyoma
Types – Serosal, intramural, submucosal (infertility, bleeding  alters endometrium)
Leiomyoma, gross, micro, tx
Gross: multiple, well circumscribed, solid white-tan nodules, whorled appearance.
Micro: fascicles of smooth muscle.
Resection, embolization, hormonal therapy.
Leiomyosarcoma epid
Perimenopausal 40s-60s
leiomyosarcoma sx
- Pelvic mass
- Vaginal bleeding
- Pelvic pain
leiomyosarcoma pathology
Gross: large, solitary, +/- hemorrhage and necrosis.
Micro: increased cellularity, mitotic figures (>10/HPF), nuclear atypia.
Hydatidiform Mole
Asia, LA, ME, 1:100 gestations, young/old pregnancies. Late first or early second trimester. Treat by curettage.
Hydatidiform Mole sx
- Abnormal bleeding
- Large uterus
- Elevated HCG.
Hydatidiform Mole

Relative androgenesis 
Complete Mole – 90% with 46XX, fertilization of an empty egg by 1 sperm (replicates) or 2 sperm  no embryonic development (DUH!)
Partial Mole – triploid 69XXY, fertilization of normal egg with 2 sperm.
Gross: edematous villi, lots of gestational tissue
Micro: Complete – single population of abnormal edematous villi, no fetal development. Partial – mixture of villi, fetal development may occur.
Choriocarcinoma epid
Rare, 1 in 20K, usually presents with mets. Death from hemorrhagic cx.

- Abnormal bleeding
- Elevated HCG
Epithelial tumor from syncytio- and cyto-trophoblast arise in endometrium.
Gross: soft pale appearance, with hemorrhage & necrosis.
Micro: invasion of myometrium and lymphovascular spaces. No villi formed. Highly sensitive to chemotherapy, high rate of cure.
Cervicitis chronic vs acute epid.
Chronic – universal, insignificant
Acute – Chlamydia, gonococci, mycomplasms, HSV.
Cervicitis pathology chronic vs acute
Chronic – squamous metaplasia in the transformation zone (post-menarche) obstructs glandular crypt openings  mucus accumulation in glands  Nabothian cysts with surrounding inflammatory response.

Acute – due to specific infx and acute inflammatory response