Pathoma (HIGH YIELD) Flashcards

(85 cards)

1
Q

Vulvar carcinoma etiologies

A

HPV (dysplasia, VIN) and non-HPV (longstanding lichen sclerosis)

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2
Q

Extramammary Paget’s disease vs Melanoma differentiation?

A

Paget’s: PAS+, keratin +, S100-

Melanoma: PAS-, keratin-, S100+

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3
Q

Vaginal carcinomas nodal metastasis pattern

A

Lower 1/3: inguinal nodes

Upper 2/3: iliac nodes

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4
Q

High risk HPV proteins

A

E6 (destruction of p53), E7 (destruction of Rb)

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5
Q

Cervical carcinoma risk factors

A

HPV (no 1), but smoking and immunodeficiency also important

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6
Q

What malignancy is an AIDS-defining illness in a woman with HIV?

A

Cervical cancer

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7
Q

Frequent cause(s) of mortality in Cervical cancer

A

“Local invasion” (e.g. invasion through bladder, hydronephrosis, renal failure)

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8
Q

Limitations of Pap smear screening

A
  • Inadequate sampling of transition zone

- Decr. efficacy in screening adenocarcinoma

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9
Q

Does HPV vaccination preclude the need for routine Pap smears? Why?

A

No; does not offer protection against HPV 31, 33

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10
Q

Asherman syndrome cause

A

Progressive amenorrhea d/t loss of basalis (regenerative layer) and scarring

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11
Q

Risk factor(s) for endometrial polyp(s)

A

Can arise as side effect of Tamoxifen

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12
Q

Define adenomyosis

A

Endometriosis of myometrium

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13
Q

Most important predictor for progression to carcinoma in Endometrial hyperplasia

A

Cellular atypia

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14
Q

Leiomyosarcoma etiology

A

De novo (does not arise from leiomyoma)

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15
Q

Describe normal endocrine regulation of ovulation in the ovary

A

LH acts on theca cells, which produce androgens, which are then converted to estradiol in the granulosa cells under the influence of FSH, eestradiol then causes egg maturation

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16
Q

Most common germ cell tumor in children

A

Endodermal sinus tumor (type of yolk sac tumor)

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17
Q

Endodermal sinus tumor lab findings

A

Elevated AFP

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18
Q

Endodermal sinus tumor lab findings

A

Elevated AFP

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19
Q

Defines Meigs syndrome

A

Ovarian fibroma (benign tumor of fibroblasts) plus pleural effusion, ascites

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20
Q

What mutation incr. risk for serous carcinoma of the ovary and fallopian tube?

A

BRCA1

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21
Q

What ovarian tumor usually contains urothelium?

A

Brenner tumor

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22
Q

Choriocarcinoma response to chemo?

A

Good response for gestational pathway (i.e. from complete mole); poor response if germ cell pathway

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23
Q

Hypospadias cause

A

Failure of urethral folds to close

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24
Q

Penile SCC precursor lesions

A
  • Bowen disease (shaft)
    • Leukoplakia on shaft of penis; has not invaded BM
  • Erythroplasia of Queyrat (glans)
  • Bowenoid papulosis (reddish papules)
    • Not true Bowen’s disease b/c it does not usually progress to invasion
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25
Testicular torsion presentation
Adolescents with acute testicular pain and absent cremasteric reflex
26
Seminoma histopathology
No hemorrhage or necrosis
27
What type of testicular tumor may form glands?
Embryonal carcinoma
28
Most common testicular tumor in children
Yolk sac tumor (aka endodermal sinus tumor)
29
Possible clinical presentation of choriocarcinoma
Gynecomastia, hyperthyroidism (both d/t elevated b-HCG)
30
Leydig cell tumor characteristic histology
Reinke crystals
31
Leydig cell tumor characteristic histology
Reinke crystals
32
Are teratomas benign or malignant?
Benign in females; potentially malignant in males
33
Acute prostatitis on DRE
Tender and boggy
34
BPH occurs in this zone of the prostate (according to Pathoma)
What is the periurethral zone
35
Prostate adenocarcinoma characteristic histology
Small glands, nuclei contain dark nucleoli
36
Growth hormone adenoma presentation
Secondary diabetes is often present
37
Sheehan syndrome cause and symptoms
Pituitary growth during pregnancy d/t more blood flow incr. susceptibility to infarct during delivery; difficulty with lactation, pubic hair loss
38
Thyroglossal duct cyst presentation
Anterior neck mass
39
Lingual thyroid presentation
Mass at base of tongue
40
Cause of incr. BMR in hyperthyroidism
Incr. synthesis of Na+/K+ ATPase
41
Cause of incr. SNS activity in hyperthyroidism
Incr. expression of beta adrenergic receptors
42
Hyperthyroidism on a lipid panel
Hypocholesterolemia
43
Enzyme most often deficient in dyshormogenetic goiter
Thyroid peroxidase (causing pediatric hypothyroidism)
44
Haplotype associated with Hashimoto thyroiditis
HLA DR5
45
Histopathologic findings in Hashimoto thyroiditis
Abundant chronic inflammation with formation of germinal centers; Hurthle cells
46
Riedel fibrosing thyroiditis presentation
Hypothyroidism with "hard as wood" nontender thyroid
47
Subacute (deQuervain) granulomatous thyroiditis presentation
Transient hyperthyroidism with tender (particularly unique) thyroid
48
How is a thyroid biopsy usually performed and why?
FNA; thyroid is (very) vascular
49
Thyroid follicular adenoma histopathology
Benign proliferation of follicles surrounded by a fibrous capsule
50
4 types of thyroid carcinomas
Papillary medullary follicular anaplastic
51
Most important risk factor for papillary thyroid carcinoma
Exposure to ionizing radiation in childhood
52
Gross appearance of follicular thyroid carcinoma; what significance does this have with respect to thyroid bx?
Extension through capsule; cannot differentiate adenoma from follicular ca on FNA
53
Medullary thyroid cancer histopathologic appearance
Malignant cells within amyloid stroma
54
Medullary thyroid cancer genetics
Mutation in RET oncogene (mutations detected in RET always prompt prophylactic thyroidectomy)
55
PTH effect on bone
Incr. osteoblast activity, which in turn incr. osteoclast activity, crushing bone, leading to Ca++ and Phosphate release
56
Primary hyperparathyroidism GI sequelae
Acute pancreatitis (most important), PUD, constipation
57
Primary hyperparathyroidism urine labs
Incr. cAMP (PTH binds tubular cells of kidney, activates Gs protein thus activating adenylate cyclase, after which incr. cAMP leaks into urine)
58
Primary hyperparathyroidism serum labs
Incr. Alk phos, incr. Ca++, incr. Phosphate, incr. PTH
59
Cause of pseudohypoparathyroidism
Defect in Gs protein
60
Why is obesity implicated in type II diabetes?
Decr. number of insulin receptors
61
Which has a stronger genetic predisposition: type I or type II diabetes?
Type II diabetes
62
Pancreatic histopathology in diabetes
Amyloid deposition in islets
63
Diabetic neuropathy pathophysiology
Schwann cells can absorb glucose independent of insulin, then aldose reductase converts to sorbitol, leading to osmotic damage
64
How can Cushing syndrome lead to HTN?
Cortisol upregulates alpha-1 receptors (cortisol is "necessary for life" b/c it maintains vascular tone)
65
Causes of chronic adrenal insufficiency
- Autoimmune (most common in West) - TB (most common in developing world) - Bilateral metastatic disease (recall unique site of metastasis for lung ca)
66
Adrenal medulla cell composition (incl. embryologic origin)
Chromaffin cells (derived from NCCs)
67
Gross appearance of pheochromocytoma
Brown
68
Pheochromocytoma diagnostic requirements
Serum metanephrines (breakdown product of epinephrine), elevated 24-hr metanephrines and VMA (breakdown product of metanephrines and normetanephrines)
69
What medication is given before pheochromocytoma removal and why?
alpha-Phenoxybenzamine (irreversible alpha-1 blocker); intraoperative compression of pheo could release massive amount of catecholamines, causing HTN surge
70
Most common location (and presentation) of pheochromocytoma outside adrenal medulla
Bladder wall (hypertensive during urination)
71
Embryologic origin of breast tissue; why is this important?
Skin (modified sweat gland); breast tissue (incl. nipples, cancer) can develop anywhere along "milk line" (axilla to vulva)
72
Normal breast tissue epithelial composition
Lobules and ducts lined by 2 layers: myoepithelial cell layer and luminal cell layer
73
Highest density of breast tissue is located where?
Upper outer quadrant(s)
74
Mammary duct ectasia symptoms
Periareolar mass, green-brown nipple discharge
75
2 possible presentations of breast fat necrosis
Mass on exam; calcifications on mammogram (higher yield)
76
Fibrocystic breast histopathology that does NOT incr. risk of cancer (in either breast)
Fibrosis, cysts, apocrine metaplasia (one of a few metaplasias that do not incr. cancer risk)
77
Fibrocystic breast histopathology that DOES incr. risk fo cancer (in either breast)
Ductal hyperplasia, sclerosis adenosis (often calcified), atypical hyperplasia
78
Intraductal papilloma (breast) vs papillary carcinoma differentiation
Papillary carcinoma won't have myoepithelial cells
79
Phyllodes tumor (breast) histopathology
Fibroadenoma-like with overgrowth of fibrous component; leaf-like projections
80
Comedo type DCIS histopathology
High grade cells, necrosis, dystrophic calcifications (i.e. calcium in dead cells) in ductal lumen
81
Medullary carcinoma (of breast) histopathology
High grade malignant cells in background of inflammatory cells (especially plasma cells and lymphocytes)
82
Medullary carcinoma (of breast) genetics
BRCA1
83
Which breast neoplasms lack E-cadherin?
LCIS; invasive lobular carcinoma
84
Invasive lobular carcinoma (of breast) histopathologic feature
Grows in single file pattern
85
Most important part of TNM staging in breast cancer prognosis
Metastasis