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Path 4 > pathology_block_4_20160207142620 > Flashcards

pathology_block_4_20160207142620 Flashcards

1
Q

greatest density of breast tissue in a female

A

upper, outer

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2
Q

most common physiologic cause of galactorrhea

A

nipple stimulation

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3
Q

most common pathologic cause of galactorrhea

A

prolactinoma

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4
Q

type of tumor that can cause gynecomastia

A

testicular choriocarcinoma

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5
Q

most common pathogenic cause of acute mastitis

A

S. aureus

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6
Q

cellular change responsible for predicate mastitis

A

keratinizing squamous metaplasia of the lactiferous ducts

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7
Q

characteristic d/c for mammary duct ectasia

A

green-brown nipple discharge

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8
Q

typical presentation of breast fat necrosis

A

incidental finding of micro calcifications on mammogram

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9
Q

what biopsy findings in fibrocystic change are associated with increased risk of cancer?

A

ductal hyperplasia- 2x sclerosing adenosis- 2xatypical hyperplasia- 5x

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10
Q

how is a papilloma differentiated from a papillary carcinoma?

A

papilloma has luminal epithelium and myoepithelial cells; carcinoma only has luminal epithelium

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11
Q

which medication is known to cause the development of multiple, bilateral fibroadenomas?

A

cyclosporin A

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12
Q

what is the characteristic biopsy finding for fibroadenoma?

A

“cave paintings’- glands become compressed due to abundant stroma

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13
Q

what is the characteristic biopsy finding for phyllodes tumor?

A

“leaf-like projections”- overgrowth of fibrous portion

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14
Q

what is the difference between fibroadenoma and phyllodes tumor? (2)

A
  • fibroadenoma is always being, phyllodes can be malignant- fibroadenoma is more common in premenopausal, phyllodes is more common in postmenopausal
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15
Q

most common breast cancer presentation

A

asymptomatic with abnormal mammogram

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16
Q

most common site for a breast cancer in females? males?

A

females- upper/outermales- subareolar

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17
Q

precursor lesion to DCIS

A

ductal hyperplasia

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18
Q

most common DCIS subtype

A

comedo (necrosis and calcifications)

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19
Q

what is Paget’s disease of the breast?

A

extension of malignancy from the duct to the skin

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20
Q

what malignancy is usually associated with Paget’s disease of the breast? exception?

A

usually DCIS, except if there is a palpable mass, then it is usually invasive carcinoma

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21
Q

4 types of invasive ductal carcinoma

A

tubular mucinousmedullaryinflammatory

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22
Q

which type of invasive ductal carcinoma is associated with BRCA1?

A

medullary

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23
Q

which type of invasive ductal carcinoma is associated with older women?

A

mucinous

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24
Q

which type of invasive ductal carcinoma is associated with the poorest prognosis?

A

inflammatory

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25
Q

what is the typical “pattern” of LCIS?

A

multifocal and bilateral

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26
Q

what “cellular defect” is associated with LCIS and invasive lobular carcinoma?

A

loss of E-cadherin (gene CDH)

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27
Q

2 unique biopsy findings for invasive lobular carcinoma

A

-single file pattern of cells - signet ring cells

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28
Q

unique mets of invasive lobular carcinoma

A

carcinomatous meningitis

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29
Q

most important prognostic factor in breast CA

A

mets

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30
Q

most useful prognostic factor in breast CA

A

spread to LN

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31
Q

which LNs are involved in spread of breast CA?

A

outer- axillary LNinner- internal mammary LN

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32
Q

treatment for ER/PR+

A

antiestrogenic - tamoxifen

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33
Q

treatment for Her2/Neu

A

trastuzumab

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34
Q

locus of BRCA1

A

17q21

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35
Q

locus of BRCA2

A

13q12.3

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36
Q

BRCA1 mutation cancers

A

breast and ovarian

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37
Q

BRCA2 mutation cancers

A

breast (males and females)

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38
Q

most common type of breast CA in males

A

invasive ductal carcinoma

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39
Q

genetic abnormalities associated with male breast CA

A

BRCA2, Klinefelters

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40
Q

fibroadenomas may grow under the influence of —

A

estrogen (during pregnancy, menstrual cycle)

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41
Q

characteristic cells in medullary carcinoma

A

lymphocytes

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42
Q

male breast cancers are mainly in the —

A

elderly

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43
Q

4 “fibrocystic changes”

A

duct proliferation, duct dilation, apocrine metaplasia, fibrosis

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44
Q

histologic appearance of gynecomastia

A

proliferation of ducts in fibrous stroma

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45
Q

characteristic histological features of HSV infection (2)

A

intranuclear inclusions (Cowdry bodies) and multinucleate giant cells

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46
Q

HPV types assoc with genital warts

A

6, 11 (low risk)

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47
Q

physical exam findings of lichen sclerosis

A

leukoplakia, parchment-like epidermis

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48
Q

lichen sclerosis has increased risk for–

A

squamous cell carcinoma

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49
Q

physical exam findings of lichen simplex chronicus

A

leukoplakia, thick/leathery epidermis

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50
Q

2 “types” of vuvlar squamous cell carcinoma

A

HPV related (16,18)non-HPV related (lichen sclerosis, p53)

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51
Q

type of vulvar SCC associated with lichen sclerosis

A

non-HPV associated

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52
Q

what is extramammary Paget’s disease

A

malignant epithelial cells in the epidermis of the vulva that presents as an erythematous/itchy/uclerated skin lesion

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53
Q

what is different between Paget’s of the nipple vs vulva?

A

nipple- assoc with underlying malignancyvuvla- no underlying malignancy

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54
Q

how is Paget’s of vulva differentiated from melanoma

A

Pagets: PAS+, keratin+melanoma: S100+

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55
Q

estrogen is responsible for ___ in vaginal epithelial cells

A

glycogenation

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56
Q

effects on DES daughters (4)

A

vaginal adenosis, clear cell carcinoma, abnormalities of smooth muscle= infertility and pregnancy loss

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57
Q

what is adenosis?

A

persistence of columnar epithelium in the upper 2/3 of the vagina, related to DES exposure

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58
Q

clear cell adenocarcinoma

A

vaginal malignancy associated with proliferations of glands with clear cytoplasm in upper 1/3 of vaginal, related to DES exposure

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59
Q

characteristic tissue/cell for embryonal rhabdomyosarcoma

A

tissue- immature skeletal muscle cell- rhabdomyoblast

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60
Q

appearance and staining of rhabdomyoblast

A

cytoplasmic cross striations (tennis racket) with + design and myogenin

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61
Q

vaginal cancer LN spread per location

A

upper 2/3- iliac nodeslower 1/3- inguinal nodes

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62
Q

ectocervix vs endocervix

A

ecto- nonkeratinizing squamous endo- columnar junction= transformation zone

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63
Q

2 common benign findings on cervical exam

A

nabothian cysts, ectropion

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64
Q

acute vs chronic cervicitis

A

acute- usually postpartum, staph or strep chronic- m/c chalmydia

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65
Q

HPV likes to infect the-

A

transformation zone

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66
Q

HPV E6 protein

A

affects p53 function, allows damaged cells to progress G1-S

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67
Q

HPV E7 protein

A

removes Rb, increasing free E2F, allowing progression G1-S

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68
Q

characteristic HPV infected cell

A

Koilocyte

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69
Q

CINs (4)

A

CIN I- under 1/3, 66% regressCIN II- under 2/3, 33% regressCIN III- under full, unlikely to regressCIS- full, will not regress

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70
Q

common cause of death in advanced cervical cancer

A

hydronephrosis with post-renal failure due to local invasion

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71
Q

3 top risk factors for cervical cancer

A

HPV infection, smoking, immune deficiency

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72
Q

somatic mutation associated with cervical cancer

A

LKB1 (Peutz-Jeghers)

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73
Q

HPV vaccine covers-

A

6,11,16,18

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74
Q

asherman syndrome

A

amenorrhea secondary to over-agressive curettage that destroys the basalis layer of the endometrium

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75
Q

anovulatory cycle

A

lack of ovulation leads to early bleeding due to lack of progesterone support

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76
Q

diagnosis of chronic endometritis requires the presence of; may result in

A

plasma cells; infertility

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77
Q

3 theories of endometriosis

A

retrograde menstruation*metaplasticlymphatic spread

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78
Q

most commonly involved site of endometriosis

A

ovary= chocolate cyst

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79
Q

endometriosis = increased risk of (2)

A

carcinoma at involved sites clear cell tumor of ovary

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80
Q

endometrial hyperplasia is due to

A

unopposed estrogen

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81
Q

what is the most important risk factor for progression of endometrial hyperplasia to carcinoma

A

presence of atypia

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82
Q

leiomyoma are __ dependent, consequences

A

estrogen; will enlarge during pregnancy/cycles and atrophy after menopause

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83
Q

m/c site for leiomyoma

A

intramural

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84
Q

leiomyosarcoma, gross findings

A

necrosis and hemorrhage

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85
Q

most common cancer of female genital tract

A

endometrial CA

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86
Q

2 pathways of endometrial CA

A

hyperplastic (75%)sporadic (25%)

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87
Q

associations with hyper plastic pathway

A

arises from pre-existing hyperplasiaassociated with unopposed estrogen PTEN mutation endometrioid spreads locally

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88
Q

associations with sporadic pathway

A

no precursorp53 mutationspsammoma bodies more aggressive

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89
Q

3 histological classifications of endometrial hyperplasia

A

simple - cystic complex- crowded atypical- crowded and atypical

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90
Q

most important factor in determining between leiomyoma and leiomyosarcoma

A

mitotic rate

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91
Q

adenomyosis can present with-

A

diffuse uterine enlargement

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92
Q

“DNA” changes associated with endometriosis

A

hypomethylation of NR5AI, ESR2

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93
Q

hydrosalpinx

A

serous fluid following resolution of infection, increased risk of infertility

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94
Q

pyosalpinx

A

purulent fluid during current infection, increased risk of infertility

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95
Q

m/c site of ectopic pregnancy

A

ampulla

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96
Q

presentation of ectopic pregnancy

A

+preg test, pelvic pain around 8 week gestation

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97
Q

risk factors for ectopic pregnancy (2)

A

previous tube damage/scarringendometriosis

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98
Q

action of LH

A

acts on theca cells, causes androgen production

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99
Q

action of FSH

A

acts on granulosa cells, causes estradiol production

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100
Q

what is the hormone imbalance in PCOS?

A

high LH, low FSH (ratio 2:1 or more)

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101
Q

why is FSH low in PCOS?

A

LH leads to production of excess androgen, excess androgen is then converted to estrone in adipose tissues, excess estrone exerts negative feedback on the ant pit = low FSH

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102
Q

most common type of ovarian tumor

A

surface epithelial tumor `

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103
Q

ovarian cystadenoma (description, more common in)

A

single cyst with simple, flat liningmore common in pre-menopausal women

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104
Q

ovarian cystadencarcinoma (description, more common in)

A

complex cyst with thick, shaggy liningmore common in postmenopausal women

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105
Q

unique mets for ovarian cystadenocarcinoma

A

omentum = omental caking

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106
Q

genetic abnormality assoc with increased risk of ovarian cystadenocardinoma

A

BRCA1 (also fallopian tube cancer)

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107
Q

lab test used to monitor response to treatment for ovarian cystadenocarcinoma

A

CA-125

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108
Q

brenner tumor

A

benign, bladder-like epithelium

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109
Q

type of ovarian cancer associated with endometriosis

A

endometrioid

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110
Q

2 types of ovarian tumors derived from fetal tissue

A

teratoma, embryonal carcinoma

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111
Q

cystic teratoma is considered malignant if (2)

A

it contains immature tissue (m/c neural) or it contains somatic malignancy (m/c SCC of skin)

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112
Q

cystic teratoma must contain

A

2/3 embryonic layers

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113
Q

struma ovarii-

A

teratoma composed of large amounts of thyroid tissue, can cause hyperthyroidism

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114
Q

embryonal carcinoma

A

malignant tumor with large, primitive cells

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115
Q

ovarian tumor composed of oocytes

A

dysgerminoma

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116
Q

dysgerminoma

A

malignant tumor composed of large cells with clear cytoplasm and central nuclei

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117
Q

male counterpart for dysgerminoma

A

seminoma

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118
Q

lab that can be elevated in dysgerminoma

A

LDH

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119
Q

ovarian tumor composed of yolk sac

A

endodermal sinus tumor

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120
Q

endodermal sinus tumors are the most common ovarian tumor in what population

A

children

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121
Q

what is the characteristic histologic finding for endodermal sinus tumors?

A

schiller-ducal bodies

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122
Q

what are the characteristic lab elevations for endodermal sinus tumors?

A

elevated AFPelevated A1AT

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123
Q

ovarian tumor composed of placental tissue

A

choriocarcinoma

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124
Q

what is the typical course for choriocarcinoma? why?

A

small primary, early mets because syncytiotrophoblasts are programmed to invade blood vessels

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125
Q

what lab is elevated in choriocarcinoma? why?

A

bHCGit is produced by syncytiotrophoblasts

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126
Q

which “pathway” for development of choriocarcinoma has a better prognosis?

A

gestational

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127
Q

granulosa-theca cell tumors make-

A

excess estrogen

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128
Q

sertoli-leydig cell tumors make-

A

excess androgen

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129
Q

presentation of granulosa-theca cell tumors

A

precocious puberty, heavy bleeding, postmenopausal bleeding

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130
Q

histologic finding for stroll-leydig cell tumors

A

reinke crystals

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131
Q

meigis syndrome

A

pleural effusions and ascites associated with fibroma of the ovary, resolves with tumor removal

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132
Q

Krukenberg tumor

A

bilateral mets to ovary

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133
Q

m/c source for Krukenberg, others

A

m/c- diffuse-type gastric adenocarcinoma, others are breast and colon

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134
Q

pseudomyxoma peritonei

A

metastatic mucinous tumor of the ovary with massive mucus accumulation in the peritoneum

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135
Q

source tumor for pseudomyxoma peritonei

A

appendix

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136
Q

ovarian fibroma cell shape

A

spindle cells

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137
Q

which 2 GYN tumors have psammoma bodies?

A

ovarian cystadenoma/carcinomaendometrial carcinoma

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138
Q

most common cause of miscarriage (especially)

A

chromosomal abnormalities, especially trisomy 16

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139
Q

general cause of pregnancy loss:0-12 weeks, 13-19 weeks, 20-24 weeks, over 25 weeks

A

0-12: chromosomal 13-19: organ specific ab20-24: inflammatory over 25: placental d/o

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140
Q

timeframe when teratogen exposure will cause organ malformation

A

weeks 3-8

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141
Q

timeframe when teratogen exposure will cause spontaneous abortion

A

weeks 1-2

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142
Q

timeframe when teratogen exposure will cause organ hypoplasia

A

months 3-9

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143
Q

teratogen that is the most common cause of mental retardation

A

alcohol

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144
Q

teratogenic effects of isotretinoin (3)

A

spont abortion, cleft lip/palate, hearing/visual impairment

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145
Q

teratogenic effects of phenytoin

A

digit hypoplasia, cleft lip/palate

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146
Q

teratogenic effect of cyclopamide

A

cycloplegia

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147
Q

immune mediated hydrous is secondary to-

A

Rh incompatability

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148
Q

placenta previa presents with

A

painless 3rd trimester bleeding

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149
Q

placental abruption presents with

A

painful 3rd trimester bleeding

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150
Q

placenta accreta presents with

A

difficulty delivering placenta after birth, post part bleeding

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151
Q

triad of pre-eclampsia

A

PIH, edema, proteinuria

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152
Q

pre-eclampsia occurs due to defects (2)

A

defects in maternal-fetal vascular interface and endothelial dysfunction

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153
Q

complications of pre-eclampsia that warrant immediate delivery

A

eclampsia- seizures HELLP- hemolysis, elevated liver enzymes, low platelets

154
Q

characteristic RBC finding in parvo B19

A

RBC inclusions

155
Q

characteristic finding in CMV

A

owl’s eye inclusions

156
Q

complete mole forms by

A

fertilization of empty egg by 2 sperm

157
Q

complete mole ploidy

A

46, all paternal

158
Q

presentation of complete mole

A

passing grape-like masses in 2nd trimester

159
Q

US of complete mole

A

snow storm, no fetal parts

160
Q

partial mole forms by

A

fertilization of normal egg by 2 sperm

161
Q

partial mole ploidy

A

69

162
Q

bHCG findings in complete vs partial mole

A

complete- high partial- normal or low

163
Q

followup after mole

A

serial bHCG x 1 year to assess for development of choriocarcinoma

164
Q

dichorionic, diamniotic, fused placenta

A

separated at 1-3 days (morula)

165
Q

monochorionic, diamniotic, fused placenta

A

separated at 4-8 days (blastula)

166
Q

monochorionic, monoamniotic, fused placenta

A

separated at days 8-13 (implanted blastocyst)

167
Q

twins that separate at what stage are at risk for being conjoined?

A

development of bilaminar disc (days 13-15)

168
Q

which type of twins are at risk for twin-twin transfusion syndrome?

A

Monochorionicdiamniotic fused placenta

169
Q

which type of twins are at risk for cord abnormalities

A

monochorionicmonoamnionicfused placenta

170
Q

malformation

A

primary defect in morphogenesis

171
Q

disruption

A

secondary disruption of normal functioning

172
Q

deformation

A

external disturbance

173
Q

sequence

A

multiple anomalies that develop from a single aberration

174
Q

malformation syndrome

A

mutliple anomalies that cannot be explained by a single aberration

175
Q

association

A

nonrandom occurrence of multiple anomalies that are not genetically linked

176
Q

hormone detected in large amounts with placental site trophoblastic tumor

A

human placental lactogen

177
Q

agenesis

A

absent organ, absent primordial tissue

178
Q

aplasia

A

absent organ, primodrial tissue present

179
Q

hypoplasia

A

incomplete organ development

180
Q

how infant is exposed to transcervical perinatal infection? disease caused

A

“inhale” in utero or via birth process; common cause of pneumonia

181
Q

how infant is exposed to trans placental perinatal infection? disease causes

A

via blood through chorionic villi, TORCH infections

182
Q

what is the underlying cause of RDS?

A

deficient surfactant

183
Q

what are the risk factors for RDS?

A

male, maternal DM, prematurity, C-section

184
Q

why is maternal DM a risk for RDS?

A

high insulin levels suppress surfactant production

185
Q

why is C-section a risk for RDS?

A

decrease in stress-induced steroid release leads to less surfactant

186
Q

what composes the hyaline membranes?

A

necrotic epithelial cells and plasma proteins

187
Q

2 complications associated with O2 therapy for RDS

A

retinopathy of prematuritybronchopulmonary dysplasia/dec septation

188
Q

what are the 2 phases of retinopathy of prematurity?

A

1- decreased VEGF/apoptosis2- increased VEGF/neovascularization

189
Q

what is the typical scenario for NEC?

A

premature infant who just started enteral feeds

190
Q

what is the characteristic Xray finding in NEC?

A

submucosal gas bubbles (pneumatosis intestinalis)

191
Q

3 presenting symptoms of NEC

A

bloody stool, abdominal distention, circulatory collapse

192
Q

definition of SIDS

A

sudden, unexpected death of infant under 1 that remains unexplained after autopsy, review of clinical hx and investigation of scene

193
Q

90% of SIDS cases occur between what ages

A

2-4 mo

194
Q

risk factors for SIDS (11)

A

young mom, smoking, male, premature, multiple, short time between babies, parental drug use, family hx SIDS, hyperthermia, soft surface, prone position

195
Q

Rh immune hydrops is due to

A

Rh incompatibility (Rh- mon, Rh+ baby)

196
Q

infant with immune hydrops will have what additional features?

A

jaundice and kernicterus (due to hemolysis)

197
Q

which antigen is the focus of immune hydrops?

A

D antigen

198
Q

why is ABO incompatibility now a more common cause of immune hydrops?

A

effective treatment of Rh with RHOgam

199
Q

what is the mother/baby problem with ABO incompatibility?

A

O type mother, A or B type fetus (may have anti-A or B IgG that can cross placenta)

200
Q

immune hydrops sensitization for Rh vs ABO

A

Rh- requiresABO- does not require, can’t affect first pregnancy

201
Q

most common infection to cause hydrops

A

parvo B19

202
Q

most common fetal anemia to cause hydrous

A

alpha thalassemia (Hb barts)

203
Q

most common benign tumor of infancy

A

hemangioma

204
Q

course for hemangiomas

A

may enlarge as child gets older, but most spontaneously regress

205
Q

most common germ cell tumor of children

A

teratoma

206
Q

neuroblastomas are composed of-

A

postganglionic sympathetic neurons

207
Q

main location of neuroblastoma

A

adrenal medulla

208
Q

labs in neuroblastoma

A

elevated urine VMA, HVA

209
Q

genetic abnormality of neuroblastoma

A

amplification of N-myc

210
Q

prognosis is based on/exception

A

based on stage (higher=worse), except for 4S (infants under 1)

211
Q

mutation assoc with retinoblastoma

A

point mutation on chromosome 13 that inactivates RB supressor gene

212
Q

patients with germ line mutation are at increased risk for-

A

osteosarcoma later in life

213
Q

why is retinoic acid teratogenic? (2)

A

down-regulation of TGFbinterferes with HOX

214
Q

ureteroplacental insufficiency will affect growth but spares the-

A

head/brain

215
Q

classic triad of congenital rubella

A

PDA, cataracts, blueberry muffin rash

216
Q

fetal alcohol syndrome presentation (4)

A

elongated philtrim, frontal bossing, heart murmur, eye problems

217
Q

first test to do if women has 3+ spontaneous abortions, followed by

A

chromosomal analysis (followed by testing for maternal antibodies/coagulopathy)

218
Q

effect of maternal DM on fetal pancreas

A

islet hyperplasia

219
Q

cells that make sufactant

A

type II pneumocytes

220
Q

L:S ratio that indicates lung maturity

A

greater than 2:1

221
Q

PKU is caused by deficiency of

A

phenylalanine hydroxylase

222
Q

presumed precursor to wilms tumor

A

nephrogenic “rests”

223
Q

NT involved in SIDS

A

serotonin (respiratory center in the medulla)

224
Q

hypospadias/due to

A

underside of penis; failure of genital folds to close

225
Q

epispadias/due to

A

dorsal surface; abnormal positioning of genital tubercle

226
Q

epispadias is associated with/increased risk for

A

bladder exstrophy/increased risk of adenocarcinoma of the bladder

227
Q

agent responsible for LGV

A

chlamydia trachomatis L1-L3

228
Q

biggest risk for penile SCC

A

uncircumsized

229
Q

bowen’s disease

A

leukoplakia on shaft or scrotum, potential to inavse

230
Q

erythroplasia of queryat

A

erythroplakia of glans, potential to invade

231
Q

bowenoid papulosis

A

multiple red papules, younger patients, NO potential to invade

232
Q

phimosis vs paraphimosis

A

phimosis- oriface is too small, cannot retractparaphimosis- partially retracted and stuck

233
Q

what promotes descent of testes into the scrotum? (2)

A

androgens and hcg

234
Q

where is the most common location of undescended testes?

A

inguinal canal

235
Q

cryptorchidism causes increased risk of?

A

seminoma (5-10x)

236
Q

mumps is more likely to cause orchitis in what age group?

A

over 10

237
Q

what is phren’s sign? suggestive of?

A

decreased pain in teste upon elevation, suggests epidiymitis

238
Q

testicular torsion is caused by

A

twisting of the spermatic cord leading to occlusion of the spermatic vein

239
Q

varicocele

A

dilation of spermatic veins = bag of worms

240
Q

comorbidity assoc with left sided varicocele

A

left sided RCC

241
Q

varicocele may increase risk of

A

infertility

242
Q

hydrocele

A

fluid in the tunica vaginalis

243
Q

unique presentation in hydrocele

A

transilluminated

244
Q

hydrocele fluid source in infants/adults

A

infants- peritoneal cavity adults- impaired lymph drainage

245
Q

appearance of testicles after mumps orchitis

A

“patchy atrophy” that can lead to infertility

246
Q

3 gene abnormalities associated with prostate CA

A

alteration of GSTP1TMPRSS2-ETS fusionPTEN

247
Q

difference in the eval of testicular tumors from other tumors

A

not biopsied due to risk of seeding scrotum

248
Q

elevated bHCG from tumors can lead to (2)

A

hyperthyroidism gynecomastia

249
Q

germ cell tumors are divided into:

A

seminomanon-seminoma

250
Q

seminoma

A

large, clear cells no hemorrhage PLAPgood prognosis

251
Q

embryonal carcinoma

A

immature/primative cells hemorrhagic early spread

252
Q

endodermal sinus (yolk sac)

A

m/c in children AFPschiller-duvall

253
Q

choriocarcinoma

A

cyto/synctiotrophoblastsbHCGsmall primary, large mets

254
Q

teratoma

A

mature fetal tissuemalignant in males

255
Q

leydig cell tumors produce/consequence; histologic feature

A

androgen= precocious puberty/gynecomastiaReinke crystals

256
Q

m/c cause of testicular mass in man over 60, 2nd m/c

A

lymphoma 2nd m/c = DLBC

257
Q

difference in labs between acute and chronic prostatitis

A

acute- WBCs, positive culturechronic: WBCs, negative culture

258
Q

m/c site of BPH

A

peri-urethral zone

259
Q

hormone that mediates prostate growth

A

DHT

260
Q

m/c complication of BPH

A

obstructive uropathy

261
Q

most important risk factor for prostate cancer

A

advancing age

262
Q

labs suggestive of prostate CA

A

elevated PSA with decreased %free

263
Q

gleason score is based only on

A

architecture

264
Q

m/c mets of prostate cancer

A

lumbar spine = osteoblastic lesions (sclerosis)

265
Q

m/c site for prostate cancer

A

peripheral zone

266
Q

most common congenital renal anomaly

A

horseshoe kidney

267
Q

3 features of Potter sequence/cause

A

flat face/low set ears lung hypoplasiaextremity defects due to oligohydraminos

268
Q

unilateral renal agenesis is associated with:

A

hyperfiltration and risk of renal failure later in life

269
Q

how is cystic renal dysplasia differentiated from polycystic kidney disease? (3)

A

CRD is usually unilateral, cysts are in parenchyma, cysts contain abnormal tissue (cartilage)

270
Q

AR PCKD gene

A

PKHD1 (fibrocystin)

271
Q

appearance of cysts in AR PCKD

A

radial, span from capsule or cortex

272
Q

extra-renal abnormalities in AR PCKD (1)

A

hepatic fibrosis/cysts

273
Q

3 presenting symptoms of AD PCKD

A

hypertension, hematuria, progressive renal failure

274
Q

AD PCKD gene

A

APKD1

275
Q

extra-renal abnormalities associated with AD PCKD

A

berry aneurysmmitral valve prolapsehepatic cysts

276
Q

m/c location of ectopic kidney, m/c complication

A

pelvis/ureter obstruction

277
Q

Pre-renal ARFcause, BUN:Cr, FENa, Urine Osm

A

decreased renal perfusion, ratio over 15, FENa under 1%, Urine Osm over 500

278
Q

Post-renal ARFcause, BUN:Cr, FENa, Urine Osm

A

obstruction of urine outflow, late = ratio ~ 15, FENa over 2%, Urine Osm under 500

279
Q

m/c cause of intra-renal ARF

A

acute tubular necrosis

280
Q

ATNcause, BUN:Cr, FENa, Urine Osm

A

ischemic or nephrotoxic cause, ratio ~ 15, FENa over 2%, urine osm under 500

281
Q

characteristic finding on urine micro in ATN

A

brown, granular casts

282
Q

most affected portion of nephron in ischemic ATN

A

PCT, TAL (require most ATP)

283
Q

most affected portion in nephrotoxic ATN

A

PCT (most exposure to agent)

284
Q

most common cause of nephrotoxic ATN

A

aminoglycosides

285
Q

acid-base abnormality associated with ATN

A

anion gap metabolic acidosis with hyperkalemia

286
Q

what is AIN?

A

drug-induced hypersensitivity reaction that damages the connective tissue between tubules

287
Q

prevention of AIN

A

fever, rash and oliguria after new med started

288
Q

characteristic finding in urine for AIN

A

eosinophils

289
Q

presentation of renal papillary necrosis

A

gross hematuria and flank pain

290
Q

predisposing to renal papillary necrosis (4)

A

analgesic abuse, DM, SCD, severe pyelo

291
Q

BP that predisposes to benign nephrosclerosis

A

SBP over 140 chronically

292
Q

typical finding in benign nephrosclerosis

A

small kidneys bilateral, hyaline arteriolosclerosis

293
Q

BP that predisposes to malignant nephrosclerosis

A

DBP over 130

294
Q

typical findings in malignant nephrosclerosis (3)

A

fibrinoid necrosis, onion skinning, flea bitten

295
Q

2 etiologies of renovascular hypertension

A

renal artery stenosis, fibromuscular dysplasia

296
Q

what is the typical patient with fibromuscular dysplasia?

A

young woman

297
Q

qualifications for nephrotic syndrome / consequences

A

urine protein over 3.5 g/dayhypoalbuminemia - edemahypogammaglobulinemia- infectionhypercoaguable state- loss of AT IIIhyperlipidemia - fatty casts

298
Q

MCD

A

m/c in kids, selective loss of albumin, due to massive cytokine release that causes effacement of foot processes, meds respond to steroids, adults may not

299
Q

gene assoc with rare cases of MCD/FSGS

A

NPHS2 (podocin)

300
Q

microscopic findings in MCD

A

EM- effacement of foot processes

301
Q

FSGS

A

m/c in AA and hispanic adults, non-selective protein loss, poor response to steroids

302
Q

associations with FSGS (3)

A

heroin, HIV, sickle cell

303
Q

microscopic findings in FSGS

A

LM- focal/segmental hyalinosis EM- effacement of foot processes

304
Q

membranous nephropathy

A

m/c in caucasian adults, autoantibodies directed at podocytes, loss of ATIII (hypercoaguable)

305
Q

associations with membranous nephropathy (5)

A

HBV, HCV, solid tumors, SLE, drugs (gold, penicillamine, NSAIDs)

306
Q

microscopic findings in membranous nephropathy

A

LM- thick glomerular BMEM- subepithelal, spike and dome IF- granular

307
Q

membranoproliferative GN “apperance”

A

tram track

308
Q

MPGN type I location of deposits, assoc

A

deposits- sub endothelial assoc- HBV, HCV

309
Q

MPGN type II location of deposits, assoc

A

deposits- intra-BMassoc- C3 nephritic factor (low serum C3)

310
Q

microscopic findings in MPGN I/II

A

LM: thick BM, hypercellular mesangiumEM: I- subendo, II- intra-BMIF: granular

311
Q

m/c cause of ESRD in the US

A

DM

312
Q

pathogenesis of diabetic nephropathy

A

high glucose leads to hyaline arteriolosclerosis, affects efferent arteriole more, hyper filtration occurs, progresses to nephrotic syndrome

313
Q

microscopic findings in DM nephropathy

A

KW nodules

314
Q

first lab elevated in DM nephropathy

A

microalbumin

315
Q

AL, AA

A

AL- blood cell dyscrasia, idiopathic AA- chronic inflammation

316
Q

microscopic findings in renal amyloidosis

A

apple green birefringence on congo-red staining

317
Q

characteristic change for diffuse proliferative GN

A

wire loop

318
Q

2 m/c causes of asymptomatic hematuria

A

IgA nephropathy, benign familial hematuria (thin BM disease)

319
Q

cells that proliferate in MPGN

A

mesangial cells

320
Q

medullary sponge kidney

A

linear striations, small cysts

321
Q

AD PKD is assoc with defects in

A

polycystin

322
Q

nephronophthisis

A

AR defect in kids. NPHP1

323
Q

characteristics of nephritic syndrome

A

inflammation and bleeding with: less than 3.5 g/day protein, salt retention/periorbital edema/HTN, azotemia, RBC casts

324
Q

what is the underlying cause of nephritic syndrome?

A

immune complexes activate complement, C5a attracts neutrophils, Neutrophils mediate damage

325
Q

typical onset of post-infectious GN

A

2-3 weeks after infection

326
Q

microscopic findings in PIGN

A

EM: subepithelial humps

327
Q

presentation of IgA nephropathy

A

hematuria 1-2 days after the onset of mucosal infection

328
Q

microscopic findings in IgA nephropathy

A

EM: immune complexes in mesangiumIf: IgA in mesangium

329
Q

defect in Alport syndrome

A

defect in type IV collagen

330
Q

triad in alport syndrome

A

hematuria, ocular defects, SN hearing loss

331
Q

most common type of renal disease in SLE

A

type IV- diffuse proliferative

332
Q

only type of RPGN that has linear IF

A

Goodpasteur

333
Q

Good pasteur: defect, symptoms, common patient

A

anti-glomerular BM antibodiesaffects lung and kindeyyoung males

334
Q

what is the characteristic LM finding for RPGN? composition? prognosis?

A

cresents (fibrin and macrophages), presence = poor prognosis

335
Q

location of deposits in DPGN

A

subendothelial

336
Q

granular IF (2)

A

post infectious GNdiffuse proliferative GN

337
Q

Pauci immune GN (3)

A

Wegners, Microscopic polyangiitis, Churg-straus

338
Q

Wegners

A

c-ANCA, nose/sinus/kidney/lungs, necrotizing granulomas

339
Q

microscopic polyangiitis

A

p-ANCA, necrotizing

340
Q

chrug-strauss

A

p-ANCA, granulomas, eosinophilia, asthma

341
Q

UTI most commonly arises from-

A

ascending infection

342
Q

gold standard of diagnosis

A

urine culture

343
Q

most common overall pathogen

A

E coli

344
Q

urethritis

A

pyuria with negative urine culture (gonorrhea, chlamydia)

345
Q

increased risk for pyelonephritis with

A

Vesicoureteral reflux

346
Q

what is the histological finding associated with chronic pyelonephritis?

A

thyroidization- atrophy of tubules with collection of proteinaceous material

347
Q

what are the most common causes of chronic pyelonephritis in children/adults?

A

children- reflux d/t abnormal VUJadults- obstruction from BPH or cervical cancer

348
Q

largest size of stone that will pass without intervention

A

5 mm

349
Q

m/c type of kidney stone

A

calcium

350
Q

m/c cause of calcium stones

A

idiopathic hypercalciuria

351
Q

drug that can help decrease occurrence of calcium stones

A

HCTZ

352
Q

type of stone associated with stag horn calculi

A

ammonium magnesium phosphate

353
Q

what type of bacteria cause AMP stones?

A

urease + (klebsiella, proteus)

354
Q

treatment of uric acid stones

A

urine alkalinization

355
Q

m/c type of stone in children

A

cysteine

356
Q

increased risk for ___ in patients with ESRD on dialysis

A

renal cell carcinoma

357
Q

cause of malakoplakia

A

chronic e coli cystitis

358
Q

findings in malakoplakia

A

in bladder- raised plaquesin kidney- PAS+ macrophages

359
Q

angiomyolipoma, association

A

hamartoma, assoc with tuberus sclerosis

360
Q

RCC is a tumor of-

A

kidney tubules

361
Q

classic triad of RCC

A

flank pain, hematuria, mass

362
Q

most common presenting symptom of RCC

A

hematuria

363
Q

5 paraneoplastic syndromes of RCC

A

epo- polycythemiaPTHrp- hypercalcemiaACTH- Cushingrenin- HTNleft varicocele

364
Q

most common histologic type of RCC

A

clear cell

365
Q

pathogenesis of clear cell RCC

A

loss of VHL (3p) = increased IGF-1 = increased HIF = increased VEGF

366
Q

sporadic clear cell RCC

A

older males, solitary mass, smoking

367
Q

hereditary clear cell RCC

A

von hippel lindau- also hemagioblastoma of the cerebellum

368
Q

gene associated with papillary RCC

A

MET

369
Q

3 cell types in a Wilm’s tumor

A

blastemaprimitive tubules stroma

370
Q

presentation of Wilm’s tumor

A

unilateral mass, hematuria, HTN

371
Q

3 syndromes assoc with Wilm’s tumor

A

WAGRDenys-DrashBeckwith-Wiedeman

372
Q

WAGR (symptoms, gene)

A

wilm’s, aniridia, genital abnormalities, retardation WT1

373
Q

Denys-Drash (symptoms, gene)

A

wilm’s, glomerular disease, male pseudohermaphroditism, WT1

374
Q

Beckwith-Wiedemann syndrome (symptoms, gene)

A

wilm’s, neonatal hypoglycemia, hemihypertrophy, organomegaly, WT2

375
Q

where is WT1? WT2?

A

WT1- 11p13WT2- 11p15.5

376
Q

risk factors for urothelial carcinoma (4)

A

smoking*, naphthylene exposure, cyclophosphamide, azo dyes

377
Q

presentation of urothelial carcinoma

A

painless hematuria

378
Q

flat type vs papillary type

A

flat- high grade flat tumor, early p53 mustpapillary- low grade, then high, no early p53

379
Q

3 things that cause SCC of the bladder

A

chronic cystitis (old female)Schistosoma hematobium (egyptian male)long standing kidney stones

380
Q

3 things that cause adenocarcinoma of the bladder

A

urachal remnantbladder exostrophycystitis glandularis

381
Q

4 types of fibrocystic changes

A

duct proliferation duct dilationapocrine metaplasiafibrosis

382
Q

3 fibrocystic changes associated with increased risk of breast CA

A

ductal hyperplasia- 2xsclerosing adenosis- 2xatypical hyperplasia- 5x

Path 4 (8 decks)

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