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Pathology Pt. 4 > Simple Deck > Flashcards

Simple Deck Flashcards

1
Q

Autosomal dominant (adult) polycystic kidney disease

A

PKD-1 and 2 –> polycystin 1 and 2

tons of fluid filled cysts, irregular surface, organ enlargement

asymptomatic until 4th decade

Clinical: flank pain, loin heaviness, liver cysts

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2
Q

Autosomal recessive (childhood) polycystic kidney disease

A

PKHD-1 –> fibrocystin

surface is smooth, radial arrangement

congenital hepatic fibrosis, too

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3
Q

Glomerulonephritis

A

immune complexes kill glomeruli

hypercellularity, glomerular necrosis

patients present with nephritic syndrome

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4
Q

Acute poststreptococcal glomerulonephritis

A

Strep Ag-Ab complexes kill glomeruli

IgG and C3 deposits

Subepithelial humps and lumps and humps and lumps

Red casts in the tubules

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5
Q

Crescentic glomerulonephritis

A

Severe glomerulonephritis

anti-type IV collagen Ab

breaks in the BM, crescents formed by proliferated parietal cells

clinical: severe, rapid nephritic syndrome

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6
Q

Goodpasture syndrome

A

Autoimmune disease that attacks collagen in the type IV collagen in the BM of lungs and kidneys, causes crescentic glomerulonephritis

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7
Q

Acute tubular necrosis

A

causes: ischemia or toxins

straight PCT and thick Henle get jacked up

proteinaceous casts of Hb and proteins in DCT and CDs

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8
Q

Acute pyelonephritis

A

cause: gram-negative bacteria; ascending or hematogenous

bacteria in urine: 100k/ml

focal lesions in kidneys

leukocyte casts in urine

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9
Q

Wilms tumor

A

large kidney tumor in children

embryonal elements/mixed tissues

90% sporadic, 10% WT1 gene

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10
Q

Renal cell carcinoma

A

malignant neoplasm of renal tubular or ductal epithelial cells

seen in older men

sporadic VHL mutation association

Clear Cell is common type: yellow-orange mass from lipid and glycogen

Clinical: hematuria, flank pain, palpable mass is the triad

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11
Q

Urothelial carcinomas

A

cancer of the bladder - transitional epithelium

cigarette smoking might cause it

clinical: sudden hematuria, dysuria

most (85%) are confined to bladder

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12
Q

GH/prolactin-secreting pituitary adenoma

A

Most common multi-hormone adenoma of the anterior pituitary

Amenorrhea, galatorrhea, loss of libido, infertility

Gigantism or acromegaly

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13
Q

Prolactinoma

A

Adenoma of the anterior pituitary that causes amenorrhea, galactorrhea, loss of libido, and infertility in women.

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14
Q

Somatotroph adenoma

A

Adenoma of the anterior pituitary that causes acromegaly or gigantism.

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15
Q

ACTH-producing adenoma

A

Adenoma of the anterior pituitary that causes Cushing syndrome, hypercortisolism, hyperpigmentation.

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16
Q

Craniopharyngioma

A

benign tumor from the remnants of Rathke’s pouch

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17
Q

Sheehan syndrome

A

hypotension from postpatrum hemorrhage –> ischemic necrosis of the pituitary

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18
Q

Cretinism

A

hypothyroidism at an early age

impaired skeletal and CNS development, coarse facial features, protruding tongue, umbilical hernia

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19
Q

Hashimoto disease

A

Goiterous hypothyroidism without iodine deficiency; autoimmune - T cells kill the thyroid gland.

Gland is diffusely enlarged, firm. Cut surface is pale tan and flashy.

Clinical features typical of hypothyroidism

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20
Q

Papillary carcinoma

A

Most common thyroid cancer type.

MAP kinase pathway activation, RET proto-oncogene mutated

Orphan Annie Eye nuclei, dense fibrovascular cores, psamonna bodies

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21
Q

Hyperparathyroidism

A

Hypersecretion of PTH from various causes - often to correct for hypocalcemia.

Clinical: hypercalcemia, bone demineralization, urinary stones, bile stones, caridiac arrhythmias.

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22
Q

Cushing syndrome

A

Adrenal hyperfunction –> lots of cortisol

Clinical: moon face, buffalo hump, skin striations

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23
Q

Addison disease

A

Adrenal hypofunction caused by autoantibody attack, TB, AIDS, or metastatic cancers.

Clinical: weakness, weight loss, GI symptoms, hyperpigmentation

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24
Q

Phaeochromocytoma

A

Neoplasm of the adrenal medulla –> tons of catecholamines

Most are sporadic, some associated with VHL disease, Multiple endocrine neoplasia (MEN)

Circumscribed nests of neoplastic cells (Zellballen).

Clinical: hypertension, tachycardia, nervousness. Dx made if catecholamines and vanillylmandelic acid are in urine.

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25
Q

Hereditary spherocytosis

A

Hemolytic anemia caused by defects in membrane proteins.

3/4 are autosomal dominant, 1/4 are AR

RBC lifespan is 10-20 days

Clinical: moderate to severe anemia, pigment stones, hemosiderosis, jaundice.

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26
Q

Sickle cell anemia

A

Hemolytic anemia due to single AA substitution in Hb B-globin chain.

Deoxy HbS –> polymerization. Repeated oxy-deoxy cycles –> calcification, destruction of RBCs.

Clinical: reticulocytosis, hyperbilirubinemia, hemosiderosis, gallstones, autosplenectomy, acute chest syndrome, stroke, vaso-occlusive (pain) crises.

Tx: hydroxyurea (increases HbF and NO)

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27
Q

Glucose-6-Phosphate dehydrogenase deficiency

A

X-linked recessive. Enzyme needed to protect RBCs against oxidation. More hemolysis occurs.

Stay away from antibiotics, large doses of aspirin, antimalarials, moth balls (napthalene), fava beans.

Bite cells, Heinz bodies.

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28
Q

Thalassemia

A

Unbalanced Hb a-globin or B-globin synthesis.

unpaired globins aggregate, kill cells

New bone formation due to marrow expansion –> crew cut skull x-ray

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29
Q

Iron deficiency anemia

A

Microcytic-hypochromic anemia caused by blood loss, diet deficiency, or increased iron demands.

Pencil/cigar-shaped cells.

Low serum iron, ferritin, transferrin. High total iron binding capacity.

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30
Q

Pernicious anemia

A

Autoimmune attack on gastric mucosa –> no intrinsic factor –> no B12 absorption –> impaired DNA synthesis –> no more new blood cells

Macrocytic-hyperchromic RBCs. CNS lesions, neuro problems (B12 only, NOT folate deficiency)

Atrophy of gastric fundic glands.

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31
Q

Polycythemia vera

A

Primary polycythemia: EPO-independent growth of RBC progenitors due to EPO receptor mutation (constitutive signaling)

Clinical: viscous blood impairs cardiac and peripheral flow, dark red skin (as with all polycythemias).

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32
Q

Chuvash polycythemia

A

Secondary polycytheima: mutated VHL increases HIF-1a stability.

Clinical: viscous blood impairs cardiac and peripheral flow, dark red skin (as with all polycythemias).

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33
Q

Prolyl hydroxylase mutations

A

The mutation causes secondary polycythemia somehow.

Clinical: viscous blood impairs cardiac and peripheral flow, dark red skin (as with all polycythemias).

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34
Q

Acute promyelocytic leukemia

A

Subtype of AML. Cancer of WBCs, causing accumulation of immature granulocytes that are blocked from differentiation due to a chromosomal translocation –> abnormal PML/RARA fusion protein.

Tx with all-trans retinoic acid

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35
Q

Chronic myelogenous leukemia

A

Cancer of WBCs. Hyperproliferation of neoplastic myeloid progenitors that retain the ability to differentiate.

Philadelphia chromosome, BCR/ABL fusion –> tyrosine kinase activation

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36
Q

Burkitt lymphoma

A

3-7 y.o, Central Africa

MYC translocation, EBV in endemic cases

large facial tumors

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37
Q

Acute lymphoblastic leukemia

A

Most common childhood leukemia. Proliferation of immature B lymphoblasts in bone marrow and peripheral blood.

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38
Q

Diffuse large B cell lymphoma

A

Most common lymphoma in adults.

Immunoblasts have prominent nucleoli.

BCL6 and BCL2 gene rearrangements.

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39
Q

Hodgkin lymphoma

A

monoclonal B lymphocyte neoplasm

Reed-Sternberg cells

staging is important

most common malignancy in Americans b/t 10-30 y.o.

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40
Q

Multiple myeloma

A

neoplasm of terminally differentiated B cells –> plasma cells

infiltrates bone marrow –> punched out skull lesions

dysregulation of D cyclin

Bence Jones protein is made (Ig component), gets to kidneys and kills kidneys –> renal failure

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41
Q

Condyloma acuminatum

A

Genital warts

HPV 6 or 11

single or multiple

with (sessile) or without stalk (pedunculated)

hyperkeratosis, epidermal thickening

koilocytosis, orderly maturation remains

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42
Q

Bowen disease

A

carcinoma in situ of penis

HPV 16

single, thick, grey-white, opaque plaque

OR

reddish plaque on glans penis = Erythoplasia of Queyrat

no orderly differentiation, BM intact

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43
Q

Bowenoid papulosis

A

The other carcinoma in situ of penis

HPV 16

multiple red-brown lesions

young, sexually active men

doesn’t develop into invasive carcinoma

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44
Q

Squamous cell carcinoma of the penis

A

Grey, crusted papular lesion on the glans penis or prepuce

infiltrates/invades the CT

25% have inguinal node involvement at Dx

5 yr survival rate is 70%

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45
Q

Cryptorchidism

A

undescended testicles

arrested germ cells

hyalinization and thickened BM

prominent Leydig cells

higher risk for testicular cancer even after Sx correction

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46
Q

Seminoma

A

Germ cell tumor of testis

most common testicular cancer; 30-40 y.o.

uniform nests and sheets of polygonal cells with central nuclei

lots of glycogen and lipid –> clear staining

25% have hCG + staining

90% cure rate

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47
Q

Acute prostatitis

A

cause: UTI bacteria

polys (neutrophils) infiltrate stroma –> microabscesses

edema, congestion

Clinical: dysuria, low back pain, pelvic pain, PSA possibly elvevated

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48
Q

Chronic prostatitis

A

glandular injury, lymphocyte infiltrate

fibroblastic proliferation

many WBCs present despite negative bacterial culture

clinical is the same as acute prostatitis: dysuria, pelvic, back pain, PSA elevated

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49
Q

Benign prostatic hyperplasia (BPH)

A

transitional or central zones

proliferation of epithelial (glandular) and stromal (fibromuscular) elements

cut surface: well-circumscribed nodules, dilated glands create cystic spaces

tall columnar cells and peripheral basal cells

compression of uretrha

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50
Q

Prostate cancer

A

peripheral zone

older folk

no basal reserve cells

Gleason grading

clinically silent, PSA may indicate but better used for recurrence indication. Metastasis to bones

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51
Q

Lichen sclerosus

A

White plaque like leukoplakia

parchment/crinkled, atrophic skin

monocyte infiltrate, hydropic degeneration, hyperkeratosis and fibrosis

Clinical: itching, dyspareunia, 1-5% –> squamous carcinoma

biopsy needed

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52
Q

Basaloid and warty carcinomas

A

HPV 16, 18

VIN (no maturation, atypia) –> squamous carcinoma

nests and cords of tightly packed squamous cells

focal central necrosis possible

warty type grows outward and has koilocytic atypia

Clinical: itching, ulcers and secondary infection

lymph spread, hemato/lymph spread to other organs common

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53
Q

Keratinizing squamous cell carcinoma of the vulva

A

NO HPV

from lichen sclerosus or squamous hyperplasia

older folk

infiltrating but normal differentiation and maturation

keratin pearls

Clinical: itching, ulcers and secondary infection

lymph spread, hemato/lymph spread to other organs common

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54
Q

Cervical intraepithelial neoplasia

A

aka dysplasia

HPV 16, 18

classification: LSIL (1/3 of epi) or HSIL (2/3)

atypia, big nuclei, hyperchromic, coarse chromatin granules, koilocytes

10% LSIL –> carcinoma

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55
Q

Squamous cell carcinoma of cervix

A

makes up 75% of cervical cancers

nests, tongues of malignant squamous epi, keratinizing or non-keratinizing, invades underlying stroma

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56
Q

Endometriosis

A

Abnormal endometrial glands + stroma outside uterus

Yellow-red = blood breakdown, red in early form

Powder burns, chocolate cysts

Found on ovaries most often

Clinical: dysmenorrhea, dyspareunia, pelvic pain

Adhesions, ectopic pregnancy

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57
Q

Endometrioid adenocarcinoma aka type 1

A

Associated with estrogen stimulation, obesity, hypertension, diabetes

mutated mismatch repair, PTEN tumor suppressor

Well (grade 1), moderately (2), poorly (3) differentiated

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58
Q

Non-endometrioid adenocarcinoma aka serous carcinoma of the endometrium aka type 2

A

happens decade later than type 1

NO estrogen association

poor differentiation, always grade 3

p53 mutation in 90%

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59
Q

Leiyomyoma

A

Very common benign tumor of uterine smooth muscle

shrinks after menopause

Firm, pale-grey, circumscribed

Can be intramural or beneath the endometrium or serosa

whorls of smooth muscle cells, foci of fibrosis, calcification, necrosis, cystic degeneration, hemorrhage.

clinical: silent, metrorrhagia, menorrhagia

60
Q

Leiyomyosarcoma

A

arises de novo from mesenchyme

uncommon

Variable morphology: bulky, polypoid lesions OR looks like leiomyoma. Variable histology.

necrotic (is best Dx criteria), soft, hemorrhagic

recurrence and lung metastasis common

5-year survival 40%

61
Q

Salpingitis

A

inflammation of fallopian tubes from lower genital tract infection

reinfection common

acute: polys, edema, congestion of mucosal folds

chronic: lymphocytes and plasma cells, no edema or congestion

late: pus and transudate distends tubes

Can lead to PID, adhesion, abscesses, infertility, ectopic pregnancy

62
Q

Surface epithelial-stromal cell tumors

A

Ovarian neoplasm associated w/ family Hx or nulliparity

HER2/NEU = poor prognosis

includes three subtypes: serous tumors, cystadenomas, cystadenocarcinomas

63
Q

Serous tumors of the ovary

A

Most frequent ovarian tumor. Large, spherical, can get huge (30-40cm)

64
Q

Cystadenoma of the ovary

A

Benign cyst of ovary.

30-40 y.o.

25% are bilateral

single layer of tall columnar epithelium

65
Q

Cystadenocarcinoma of the ovary

A

Malignant ovarian tumor

45-65 y.o.

Clinical: asymptomatic until huge, seeding, regional lymph spread common, NO distant metastasis

CA-125 marker

Bad prognosis.

66
Q

Breast cancer

A

Most common malignancy in women, 2nd leading cause of cancer death

BRCA1, 2, p53 are hereditary factors but most are sporadic

Hormonal status is big factor (late/no pregnancy increases risk)

HER2/NEU = poor prognosis

67
Q

BRCA2

A

found in 20% of hereditary breast cancer cases

carriers have 30-50% lifetime chance of getting breast cancer

Ashkenazi Jewish Women

Men are at increased risk for breast cancer, too

68
Q

BRCA1

A

mutated in 1 in 200-400 peeps in US

60-85% lifetime risk of breast cancer, increases risk for

also found in 20% of hereditary cases (like BRCA2)

not seen in sporadic cases

69
Q

Ductal carcinoma in situ (DCIS)

A

Most common in situ breast carcinoma - noninvasive

No BM penetration

Invades the shit out of ducts. Fills, distorts, unfolds lobules

Necrosis depends on subtype, calcifications

two subtypes: comedo, non-comedo

70
Q

DCIS Non-comedo subtype

A

No desmoplastic response (hardening) = no palpable or radiologically detectable mass

Nipple discharge may develop

1/3 –> carcinoma in the same breast and quadrant

Excellent prognosis

71
Q

DCIS comedo subtype (high grade)

A

Aggressive DCIS: large, pleomorphic cells, abundant cytoplasm, irregular nuclei.

Intraductal necrosis, calcification can show up radiologically

Desmoplastic response

72
Q

Lobar carcinoma in situ (LCIS)

A

2nd most common form of in situ breast carcinoma

BM intact

cells are smaller, uniform, round, regular nuclei, small nucleoli

cells don’t pack up ducts as much as DCIS

signet ring cells

no calcification

1/3 –> invasive carcinoma, used as breast cancer marker

73
Q

Invasive ductal carcinoma

A

called this b/c they can’t be categorized

associated with DCIS

irregular margins, lymph-vascular invasion, nerve invasion

nipple dimpling and retraction, nodules, breast inflammation

paraneoplastic syndrome –> hypercalcemia

hard, palpable mass due to desmoplastic response

HER2/NEU is bad

74
Q

PKD-1 and 2 –> polycystin 1 and 2

tons of fluid filled cysts, irregular surface, organ enlargement

asymptomatic until 4th decade

Clinical: flank pain, loin heaviness, liver cysts

A

Autosomal dominant (adult) polycystic kidney disease

75
Q

PKHD-1 –> fibrocystin

surface is smooth, radial arrangement

congenital hepatic fibrosis, too

A

Autosomal recessive (childhood) polycystic kidney disease

76
Q

immune complexes kill glomeruli

hypercellularity, glomerular necrosis

patients present with nephritic syndrome

A

Glomerulonephritis

77
Q

Strep Ag-Ab complexes kill glomeruli

IgG and C3 deposits

Subepithelial humps and lumps and humps and lumps

Red casts in the tubules

A

Acute poststreptococcal glomerulonephritis

78
Q

Severe glomerulonephritis

anti-type IV collagen Ab

breaks in the BM, crescents formed by proliferated parietal cells

clinical: severe, rapid nephritic syndrome

A

Crescentic glomerulonephritis

79
Q

Autoimmune disease that attacks collagen in the type IV collagen in the BM of lungs and kidneys, causes crescentic glomerulonephritis

A

Goodpasture syndrome

80
Q

causes: ischemia or toxins

straight PCT and thick Henle get jacked up

proteinaceous casts of Hb and proteins in DCT and CDs

A

Acute tubular necrosis

81
Q

cause: gram-negative bacteria; ascending or hematogenous

bacteria in urine: 100k/ml

focal lesions in kidneys

leukocyte casts in urine

A

Acute pyelonephritis

82
Q

large kidney tumor in children

embryonal elements/mixed tissues

90% sporadic, 10% WT1 gene

A

Wilms tumor

83
Q

malignant neoplasm of renal tubular or ductal epithelial cells

seen in older men

sporadic VHL mutation association

Clear Cell is common type: yellow-orange mass from lipid and glycogen

Clinical: hematuria, flank pain, palpable mass is the triad

A

Renal cell carcinoma

84
Q

cancer of the bladder - transitional epithelium

cigarette smoking might cause it

clinical: sudden hematuria, dysuria

most (85%) are confined to bladder

A

Urothelial carcinomas

85
Q

Most common multi-hormone adenoma of the anterior pituitary

Amenorrhea, galatorrhea, loss of libido, infertility

Gigantism or acromegaly

A

GH/prolactin-secreting pituitary adenoma

86
Q

Adenoma of the anterior pituitary that causes amenorrhea, galactorrhea, loss of libido, and infertility in women.

A

Prolactinoma

87
Q

Adenoma of the anterior pituitary that causes acromegaly or gigantism.

A

Somatotroph adenoma

88
Q

Adenoma of the anterior pituitary that causes Cushing syndrome, hypercortisolism, hyperpigmentation.

A

ACTH-producing adenoma

89
Q

benign tumor from the remnants of Rathke’s pouch

A

Craniopharyngioma

90
Q

hypotension from postpatrum hemorrhage –> ischemic necrosis of the pituitary

A

Sheehan syndrome

91
Q

hypothyroidism at an early age

impaired skeletal and CNS development, coarse facial features, protruding tongue, umbilical hernia

A

Cretinism

92
Q

Goiterous hypothyroidism without iodine deficiency; autoimmune - T cells kill the thyroid gland.

Gland is diffusely enlarged, firm. Cut surface is pale tan and flashy.

Clinical features typical of hypothyroidism

A

Hashimoto disease

93
Q

Most common thyroid cancer type.

MAP kinase pathway activation, RET proto-oncogene mutated

Orphan Annie Eye nuclei, dense fibrovascular cores, psamonna bodies

A

Papillary carcinoma

94
Q

Hypersecretion of PTH from various causes - often to correct for hypocalcemia.

Clinical: hypercalcemia, bone demineralization, urinary stones, bile stones, caridiac arrhythmias.

A

Hyperparathyroidism

95
Q

Adrenal hyperfunction –> lots of ACTH release

Clinical: moon face, buffalo hump, skin striations

A

Cushing syndrome

96
Q

Adrenal hypofunction caused by autoantibody attack, TB, AIDS, or metastatic cancers.

Clinical: weakness, weight loss, GI symptoms, hyperpigmentation

A

Addison disease

97
Q

Neoplasm of the adrenal medulla –> tons of catecholamines

Most are sporadic, some associated with VHL disease, Multiple endocrine neoplasia (MEN)

Circumscribed nests of neoplastic cells (Zellballen).

Clinical: hypertension, tachycardia, nervousness. Dx made if catecholamines and vanillylmandelic acid are in urine.

A

Phaeochromocytoma

98
Q

Hemolytic anemia caused by defects in membrane proteins.

3/4 are autosomal dominant, 1/4 are AR

RBC lifespan is 10-20 days

Clinical: moderate to severe anemia, pigment stones, hemosiderosis, jaundice.

A

Hereditary spherocytosis

99
Q

Hemolytic anemia due to single AA substitution in Hb B-globin chain.

Deoxy HbS –> polymerization. Repeated oxy-deoxy cycles –> calcification, destruction of RBCs.

Clinical: reticulocytosis, hyperbilirubinemia, hemosiderosis, gallstones, autosplenectomy, acute chest syndrome, stroke, vaso-occlusive (pain) crises.

Tx: hydroxyurea (increases HbF and NO)

A

Sickle cell anemia

100
Q

X-linked recessive. Enzyme needed to protect RBCs against oxidation. More hemolysis occurs.

Stay away from antibiotics, large doses of aspirin, antimalarials, moth balls (napthalene), fava beans.

Bite cells, Heinz bodies.

A

Glucose-6-Phosphate dehydrogenase deficiency

101
Q

Unbalanced Hb a-globin or B-globin synthesis.

unpaired globins aggregate, kill cells

New bone formation due to marrow expansion –> crew cut skull x-ray

A

Thalassemia

102
Q

Microcytic-hypochromic anemia caused by blood loss, diet deficiency, or increased iron demands.

Pencil/cigar-shaped cells.

Low serum iron, ferritin, transferrin. High total iron binding capacity.

A

Iron deficiency anemia

103
Q

Autoimmune attack on gastric mucosa –> no intrinsic factor –> no B12 absorption –> impaired DNA synthesis –> no more new blood cells

Macrocytic-hyperchromic RBCs. CNS lesions, neuro problems (B12 only, NOT folate deficiency)

Atrophy of gastric fundic glands.

A

Pernicious anemia

104
Q

Primary polycythemia: EPO-independent growth of RBC progenitors due to EPO receptor mutation (constitutive signaling)

Clinical: viscous blood impairs cardiac and peripheral flow, dark red skin (as with all polycythemias).

A

Polycythemia vera

105
Q

Secondary polycytheima: mutated VHL increases HIF-1a stability (for angiogenesis).

Clinical: viscous blood impairs cardiac and peripheral flow, dark red skin (as with all polycythemias).

A

Chuvash polycythemia

106
Q

The mutation causes secondary polycythemia somehow.

Clinical: viscous blood impairs cardiac and peripheral flow, dark red skin (as with all polycythemias).

A

Prolyl hydroxylase mutations

107
Q

Subtype of AML. Cancer of WBCs, causing accumulation of immature granulocytes that are blocked from differentiation due to a chromosomal translocation –> abnormal PML/RARA fusion protein.

Tx with all-trans retinoic acid

A

Acute promyelocytic leukemia

108
Q

Cancer of WBCs. Hyperproliferation of neoplastic myeloid progenitors that retain the ability to differentiate.

Philadelphia chromosome, BCR/ABL fusion –> tyrosine kinase activation

A

Chronic myelogenous leukemia

109
Q

3-7 y.o, Central Africa

MYC translocation, EBV in endemic cases

large facial tumors

A

Burkitt lymphoma

110
Q

Most common childhood leukemia. Proliferation of immature B lymphoblasts in bone marrow and peripheral blood.

A

Acute lymphoblastic leukemia

111
Q

Most common lymphoma in adults.

Immunoblasts have prominent nucleoli.

BCL6 and BCL2 gene rearrangements.

A

Diffuse large B cell lymphoma

112
Q

monoclonal B lymphocyte neoplasm

Reed-Sternberg cells

staging is important

most common malignancy in Americans b/t 10-30 y.o.

A

Hodgkin lymphoma

113
Q

neoplasm of terminally differentiated B cells –> plasma cells

infiltrates bone marrow –> punched out skull lesions

dysregulation of D cyclin

Bence Jones protein is made (Ig component), gets to kidneys and kills kidneys –> renal failure

A

Multiple myeloma

114
Q

Genital warts

HPV 6 or 11

single or multiple

with (sessile) or without stalk (pedunculated)

hyperkeratosis, epidermal thickening

koilocytosis, orderly maturation remains

A

Condyloma acuminatum

115
Q

carcinoma in situ of penis

HPV 16

single, thick, grey-white, opaque plaque

OR

reddish plaque on glans penis = Erythoplasia of Queyrat

no orderly differentiation, BM intact

A

Bowen disease

116
Q

The other carcinoma in situ of penis

HPV 16

multiple red-brown lesions

young, sexually active men

doesn’t develop into invasive carcinoma

A

Bowenoid papulosis

117
Q

Grey, crusted papular lesion on the glans penis or prepuce

infiltrates/invades the CT

25% have inguinal node involvement at Dx

5 yr survival rate is 70%

A

Squamous cell carcinoma of the penis

118
Q

undescended testicles

arrested germ cells

hyalinization and thickened BM

prominent Leydig cells

higher risk for testicular cancer even after Sx correction

A

Cryptorchidism

119
Q

Germ cell tumor of testis

most common testicular cancer; 30-40 y.o.

uniform nests and sheets of polygonal cells with central nuclei

lots of glycogen and lipid –> clear staining

25% have hCG + staining

90% cure rate

A

Seminoma

120
Q

cause: UTI bacteria

polys (neutrophils) infiltrate stroma –> microabscesses

edema, congestion

Clinical: dysuria, low back pain, pelvic pain, PSA possibly elvevated

A

Acute prostatitis

121
Q

glandular injury, lymphocyte infiltrate

fibroblastic proliferation

many WBCs present despite negative bacterial culture

clinical is the same as acute prostatitis: dysuria, pelvic, back pain, PSA elevated

A

Chronic prostatitis

122
Q

transitional or central zones

proliferation of epithelial (glandular) and stromal (fibromuscular) elements

cut surface: well-circumscribed nodules, dilated glands create cystic spaces

tall columnar cells and peripheral basal cells

compression of uretrha

A

Benign prostatic hyperplasia (BPH)

123
Q

peripheral zone

older folk

no basal reserve cells

Gleason grading

clinically silent, PSA may indicate but better used for recurrence indication. Metastasis to bones

A

Prostate cancer

124
Q

White plaque like leukoplakia

parchment/crinkled, atrophic skin

monocyte infiltrate, hydropic degeneration, hyperkeratosis and fibrosis

Clinical: itching, dyspareunia, 1-5% –> squamous carcinoma

biopsy needed

A

Lichen sclerosus

125
Q

HPV 16, 18

VIN (no maturation, atypia) –> squamous carcinoma

nests and cords of tightly packed squamous cells

focal central necrosis possible

warty type grows outward and has koilocytic atypia

Clinical: itching, ulcers and secondary infection

lymph spread, hemato/lymph spread to other organs common

A

Basaloid and warty carcinomas

126
Q

NO HPV

from lichen sclerosus or squamous hyperplasia

older folk

infiltrating but normal diff and maturation

keratin pearls

Clinical: itching, ulcers and secondary infection

lymph spread, hemato/lymph spread to other organs common

A

Keratinizing squamous cell carcinoma of the vulva

127
Q

aka dysplasia

HPV 16, 18

classification: LSIL (1/3 of epi) or HSIL (2/3)

atypia, big nuclei, hyperchromic, coarse chromatin granules, koilocytes

10% LSIL –> carcinoma

A

Cervical intraepithelial neoplasia

128
Q

makes up 75% of cervical cancers

nests, tongues of malignant squamous epi, keratinizing or non-keratinizing, invades underlying stroma

A

Squamous cell carcinoma of cervix

129
Q

Abnormal endometrial glands + stroma outside uterus

Yellow-red = blood breakdown, red in early form

Powder burns, chocolate cysts

Found on ovaries most often

Clinical: dysmenorrhea, dyspareunia, pelvic pain

Adhesions, ectopic pregnancy

A

Endometriosis

130
Q

Associated with estrogen stimulation, obesity, hypertension, diabetes

mutated mismatch repair, PTEN tumor suppressor

Well (grade 1), moderately (2), poorly (3) differentiated

A

Endometrioid adenocarcinoma aka type 1

131
Q

happens decade later than type 1

NO estrogen association

poor differentiation, always grade 3

p53 mutation in 90%

A

Non-endometrioid adenocarcinoma aka serous carcinoma of the endometrium aka type 2

132
Q

Very common benign tumor of uterine smooth muscle

shrinks after menopause

Firm, pale-grey, circumscribed

Can be intramural or beneath the endometrium or serosa

whorls of smooth muscle cells, foci of fibrosis, calcification, necrosis, cystic degeneration, hemorrhage.

clinical: silent, metrorrhagia, menorrhagia

A

Leiyomyoma

133
Q

arises de novo from mesenchyme

uncommon

Variable morphology: bulky, polypoid lesions OR looks like leiomyoma. Variable histology.

necrotic (is best Dx criteria), soft, hemorrhagic

recurrence and lung metastasis common

5-year survival 40%

A

Leiyomyosarcoma

134
Q

inflammation of fallopian tubes from lower genital tract infection

reinfection common

acute: polys, edema, congestion of mucosal folds

chronic: lymphocytes and plasma cells, no edema or congestion

late: pus and transudate distends tubes

Can lead to PID, adhesion, abscesses, infertility, ectopic pregnancy

A

Salpingitis

135
Q

Ovarian neoplasm associated w/ family Hx or no birth/>35

HER2/NEU = poor prognosis

includes three subtypes: serous tumors, cystadenomas, cystadenocarcinomas

A

Surface epithelial-stromal cell tumors

136
Q

Most frequent ovarian tumor. Large, spherical, can get huge (30-40cm)

A

Serous tumors of the ovary

137
Q

Benign cyst of ovary.

30-40 y.o.

25% are bilateral

single layer of tall columnar epithelium

A

Cystadenoma of the ovary

138
Q

Malignant ovarian tumor

45-65 y.o.

Regional lymph spread, NO distant metastasis

CA-125 marker

Clinical: asymptomatic until huge, seeding common

Bad prognosis.

A

Cystadenocarcinoma of the ovary

139
Q

Most common malignancy in women, 2nd leading cause of cancer death

BRCA1, 2, p53 are hereditary factors but most are sporadic

Hormonal status is big factor (late/no pregnancy increases risk)

HER2/NEU = poor prognosis

A

Breast cancer

140
Q

found in 20% of hereditary breast cancer cases

carriers have 30-50% lifetime chance of getting breast cancer

Ashkenazi Jewish Women

Men are at increast risk for breast cancer, too

A

BRCA2

141
Q

mutated in 1 in 200-400 peeps in US

60-85% lifetime risk of breast cancer, increases risk for

also found in 20% of hereditary cases (like BRCA2)

not seen in sporadic cases

A

BRCA1

142
Q

Most common in situ breast carcinoma - noninvasive

No BM penetration

Invades the shit out of ducts. Fills, distorts, unfolds lobules

Necrosis depends on subtype, calcifications

two subtypes: comedo, non-comedo

A

Ductal carcinoma in situ (DCIS)

143
Q

No desmoplastic response (hardening) = no palpable or radiologically detectable mass

Nipple discharge may develop

1/3 –> carcinoma in the same breast and quadrant

Excellent prognosis

A

DCIS Non-comedo subtype

144
Q

Aggressive DCIS: large, pleomorphic cells, abundant cytoplasm, irregular nuclei.

Intraductal necrosis, calcification can show up radiologically

Desmoplastic response

A

DCIS comedo subtype (high grade)

145
Q

2nd most common form of in situ breast carcinoma

BM intact

cells are smaller, uniform, round, regular nuclei, small nucleoli

cells don’t pack up ducts as much as DCIS

signet ring cells

no calcification

1/3 –> invasive carcinoma, used as breast cancer marker

A

Lobar carcinoma in situ (LCIS)

146
Q

called this b/c they can’t be categorized

associated with DCIS

irregular margins, lymph-vascular invasion, nerve invasion

nipple dimpling and retraction, nodules, breast inflammation

paraneoplastic syndrome –> hypercalcemia

hard, palpable mass due to desmoplastic response

HER2/NEU is bad

A

Invasive ductal carcinoma

Pathology Pt. 4 (10 decks)

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