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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: T
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 +/-
CD19+/-
CD20+
Burkittâ€™s B cell Lymphoma Epidemiology: 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: indolent
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: TdT+
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: indolent

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: Lymphadenopathy

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

Angiogenesis

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: CD30+
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: <5%
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: 5%
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: monocytes
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
60s

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+
esterase+
MPO+
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

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) â€“ good â€“ less chemo - kids
-(BCR/ABL) â€“ poor â€“ more chemo - adults
(CD19+, CD10+, TdT+)
Chronic Lymphocytic Leukemia Small Lymphoblastic Lymphoma Epidemiology: Most common in western world.
~65 y.o.
Indolent, 7 y
Chronic Lymphocytic Leukemia Small Lymphoblastic Lymphoma Clinical presentation: - Often asymptomatic
- Fatigue
- Anemia, infections
- Hepatosplenomegaly, lymphadenopathy
- Hypo-gammaglobulinemia
- WBC 10K â€“ 300K
Chronic Lymphocytic Leukemia Small Lymphoblastic Lymphoma biochemical pathogenesis: Mutated Ig V genes ïƒ better prognosis. Cytogenic abnormalities: trisomy 12, del 13q14, del 11q22-23 present. Prolymphocytic â€“ larger lymphocytes with a nucleolus transf (15-30%), Richter â€“ large B cell lymphoma- transf (10%)
Chronic Lymphocytic Leukemia Small 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 Small 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 epidemiology: 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 â€“ hypercellular, blasts <10%
- Peripheral â€“ myeloblasts <2%
- Absolute basophilia
- 9:22
Accelerated Phase:
- BM/Peripheral â€“ myeloblasts <20%
- Peripheral basophilia >20%
- Leukocytosis, splenomegaly
- more cytogenic abnormalities
Blast Phase:
- BM â€“ blasts >20%
- 70% myeloid blast crisis - AML
- 30% lymphoid blast crisis - ALL
Leukamoid Reaction vs. CML WBC count Toxic PMNs Basophilia Nucleus RBC Platelets: 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 Fever LAP Karyotype: 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 Cellularity M:E Ratio Megakaryos 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 â€“ refractory anemia, normal blasts, +/- sideroblasts, 6 y.
High grade â€“ refractory anemia w/ excess blasts, chemo/radioation history, multiple cytogenetic abnormalities, 6-8 mo.
myelodysplastic syndrome histological appearance Marrow Erythroid granulocytes platelets: - Hypercellular marrow, cells with dysplastic morphology
- Peripheral cytopenias
1. Erythroid â€“ dyssenchronous maturation of nucleus and cytoplasm, abnormal nuclear lobulation, multinucleated cells, ringed sideroblasts (iron granules in cytoplasmic periphery).
2. Granulocyte â€“ bilobed neutrophils (Pelger-Huet cells), no cytoplasmic granules
3. Platelets â€“ no granules, cells maybe huge (Giant platelets).
myelodysplastic syndrome treatment: supportive, BM transplant not for older pt's
Polycythemia Vera epidemiology: 10/mil
60y
M
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 Epidemiology: 1/100K 70 y
m=f
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 epidemiology: 2/100K
50s
women can presnt mid 30s
indolent
essential thrombocythenia clinical: - 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 â€“ 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 â€“ bence jones/monoclonal Ig
infectinos of esophagus: Fungal â€“ debilitated patients, Candida
Viral â€“ leukemia/lymphoma patients, HSV, CMV
Bacterial â€“ 2Âº site in lung infections
esophagitis presentation: - Dysphagia, pain, dyspepsia
- Bleeding, stricture, Barrettâ€™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
Black>W
EtOH, smoking
achalasia, stricture, esophageal stricture
not genetic
27% at 5 yrs
esophageal squamous cell carcinoma sx: dysphagia
pain
weight loss, anorexia
fatigue
ulceration/bleeding
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%, Barrettâ€™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 Barrettâ€™s esophagus with high grade dysplasia, cells resemble intestines, but can look like cells found anywhere along the GI tract.
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 â€“ H. pylori + lots of PMNs
- Chronic superficial gastritis â€“ H. pylori + lymphocytes/plasma cells
- Chronic atrophic gastritis â€“ atrophy of gastric glands
- Autoimmune â€“ fundus
- H. pylori â€“ antrum

- Hypochloridia (due to loss of parietal cells ~ autoimmune)
- Ulceration
- Gastric Carcinoma
Chronic Gastritis pathogenesis: H. pylori â€“ G-, spiral rod, acute/chronic gastritis + carcinoma. Produces urease ïƒ damages mucosal barrier ïƒ 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 ïƒ 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 â€“ aspirin, steroids, nsaids, etoh, coffee, cola, smoke, cirrhosis, copd, CRF, hypercalcemia, h. pylori toxins, changes in gastric secretions.
Chronic Peptic Ulcer Disease clinical: - Bleeding â€“ most common cause of upper GI bleeds (minor ïƒ massive)
- Perforation â€“ 5%, high mortality
- Obstruction â€“ in pyloric or duodenal ulcers
- Pain â€“ recurrent
- Cancer â€“ 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 â€“ ant/post wall 1st seg, 2nd seg
Stomach â€“ antrum, lesser curvature.
Meckels, lower esophagus, anastomatotic ulcers.

Duodenal Ulcers: hypersecretion of acid & pepsin (~parietal # â†‘, 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 â€“ patients in ICU, up to 10%.
Brain â€“ Cushingâ€™s
Burns â€“ Curlingâ€™s
Shock & Sepsis
Trauma
Aspirin & NSAIDs
Acute Gastric Ulcers: - Bleeding (minimal to massive)
- Pain (masked)
Acute gastric ulcers pathogenesis: In Some â€“ 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
Menetrierâ€™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 epi histo gross prognosis: Less common than colonic polyps, incidental, in chronic gastritis setting. Polyps are made of elongated and hyperplastic foveolar epithelium.
Adenomas â€“ rare, <10% of polyps, sessile or pedunculated, antrum. Large may progress to adenocarcinoma.
Gastric Carcinoma linitis plastica vs intestinal vs diffuse: Linitis plastica â€“ flat, spreading lesion, walls are thick, hard to diagnose.
Intestinal ~ colon adenocarcinoma, glandular formations, H. pylori, down in western world.
Diffuse â€“ cells from native gastric glands, no metaplasia.
gastric carcinoma parts of stomach %s: Pylorus, antrum â€“ 55%
Cardia â€“ 25%
Rest â€“ 20%
Gastric Mesenchymal tumors pathogenesis: Spindle cell neoplasms, from the wall of the somach (Interstital cells of Cajal â€“ pacemaker cells). Used to be called leiomyomas and leiomyosarcomas -> gastrointestinal stromal tumors.
Causes of pancreatic insufficiency: cystic fibrosis, pancreatitis â€“> loss of pancreatic enzymes
Whippleâ€™s disease: hypersensitivity to gluten â€“ gliadin, component of gluten, in grains causes immunologic flattening of villi, increased risk for T cell lymphoma and adenocarcinoma of small intestine
Lymphangiectasia: congenital â€“ 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 â€“ S aureus, Vibrios (cholera), C. perfringens
Ingestion of bacteria â€“ E.coli, Campylobacter
Ingestion of enterinvasive bacteria â€“ 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).
Omphalocele: failure of development of anterior abdominal wall, gut covered by peritoneal membrane.
Gastroschisis: 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.
Meckelâ€™s: 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) â€“ 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 â€“ 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
Crohnâ€™s Disease epid: 3/100K, F>M, Jews, 15-20 & 55-65 y, 40% family history. abnormal immune activation of T cells. SB â€“ 40%, SB LB â€“ 30%, LB â€“ 30%.
Crohn's clinical comp, presentation: Localized â€“ fistulas (10-15%), hemorrhage, strictures, risk of malignancy (2%)
Systemic â€“ 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, â€œcreeping fatâ€, 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 â€“ toxic megacolon -> perforation w/ 30% mortality, hemorrhage, stricture, carcinoma risks increase if UC is chronic, w/ multiple recurrences and is extensive. Systemic â€“ 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 â€“ 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) â€“ 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 â€“ 20%, abscess formation
- Fistula â€“ 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 â€“ 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
Neoplastic
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.
5-HIAA
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)
50K/year,recurrence
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
- â€˜Field Effect
Bladder papilloma vs carcinoma: Papilloma â€“ benign, papillary arch, normal urothelium, rare, younger patients, do not progress.
Carcinoma â€“ 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 â€“ follow
LP invasion - Alkylating agents, attenuated mycobacterium BCG (necrotizing granuloma response),
Deep LP invasion â€“ cystectomy
Metastatic - chemo
Mesenchymal Bladder Tumors peds vs adults; tx: Peds â€“ 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
W>AF
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 donâ€™t cause enlargement. Hemorrhagic and necrotic areas. Grow faster than blood supply -> fibrous scar + mets.
choriocarcinoma micro: Micro: Syncytiotrophoblastic cell â€“ large, multinucleate, vacuolated pink cytoplasm. Cytotrophoblastic cell â€“ 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
Symptoms-60s
Worldwide
Age, androgen metabolism
DRE â€“ 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

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Number of cards 248