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Intro to Disease > Exam 3: Ch. 16-20 > Flashcards

Exam 3: Ch. 16-20 Flashcards

1
Q

main function of breasts

A

milk production

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2
Q

two main types of breast tissue

A

glandular tissue-lobules and ducts

stromal tissue-supporting tissue

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3
Q

stromal tissue

A

fatty and fibrous connective tissue that gives breasts size, shape, and support

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4
Q

structure of breast

A

20 lobes of glandular tissue, each made of cluster of milk producing lobules which are connected to the nipple by branching ducts

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5
Q

suspensory ligaments

A

bands of fibrous tissue extending from skin to connective tissue covering chest wall muscles

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6
Q

where do lymph vessels in the breast lead to?

A

axillary nodes (near armpit), if cancer cells reach here the nodes swell and the cancer is more likely to spread

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7
Q

what happens to breasts during puberty?

A

they enlarge in response to estrogen and progesterone

  • glandular and fibrous tissue proliferates
  • adipose tissue accumulates
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8
Q

what happens to breasts during menstrual cycle?

A

responds to hormonal stimulation, they experience hyperplasia (growth) and involution (shrinking) in a cycle

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9
Q

what happens to breasts during pregnancy?

A

the glandular and ductal tissues are hypertrophic (cell size increases)

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10
Q

what happens to breasts after menopause?

A

sex hormone levels decline, so the breasts gradually decrease in size

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11
Q

clinical breast exam

A

-inspection, palpation, examination of axillary tissues
-first w/ arms at sides
-next w/ arms elevated, then lowered
last w/ hands on hips

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12
Q

palpation of breasts should begin where?

A

periphery of breast and in clockwise direction

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13
Q

mammogram

A

x-ray examination to identify lesions that can’t be detected on a clinical examination

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14
Q

baseline age of first mammogram?

A

35-40, or earlier if family history is present

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15
Q

when should you get a mammogram annually?

A

at age 40 and after

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16
Q

a mammogram is most useful for what population?

A

postmenopausal women, because their breasts contain more fat and less glandular tissue
-a tumor will contrast more sharply with the fatty tissue (less dense)

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17
Q

more dense masses show as what color on a mammogram?

A

white

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18
Q

less dense masses show as what color on a mammogram?

A

dark

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19
Q

cysts and benign tumors are well or poorly circumscribed?

A

well circumscribed, usually even borders and differ sharply from cells around them

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20
Q

malignant tumors usually are what?

A

poorly circumscribed, irregular borders and fine flecks of calcium

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21
Q

why may MRI be better than a mammogram?

A

it detects small carcinomas better and non-significant breast changes

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22
Q

accessory breast/nipple

A

common sites include armpit or lower chest below and medial to normal breasts-when an extra nipple forms

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23
Q

unequal development

A

fully developed breasts are usually not exactly the same, one usually fails to develop as much

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24
Q

breast hypertrophy

A

puberty; one or both breasts over-respond to hormonal stimulation and results from overgrowth of fibrous tissue

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25
Q

gynecomastia

A

ductal and fibrous tissue of an adolescent male proliferates from a temporary imbalance of female and male hormones at puberty (formation of small female breasts)

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26
Q

benign cystic change

A

very common, also called fibrocystic disease
-where focal areas of proliferation of glandular and fibrous tissue are present our to irregular cyclic response to hormones

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27
Q

what diagnoses a benign cystic change

A

ultrasound, distinguishes cystic from solid mass

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28
Q

treatment for benign cystic change

A

aspiration of cyst (removal of fluid via needle)

surgical excision

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29
Q

fibroadenoma

A

benign, well circumscribed tumor of the fibrous and glandular tissue that is common in young women and surgically removed

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30
Q

risk factors for breast carcinoma

A

family history (mother or sister), hormonal factors, first pregnancy after age 30, early menarche (1st period), late menopause, occurs in 1/10 women

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31
Q

progestin

A

synthetic compound with progesterone activity, often given with estrogen in combined hormone therapy

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32
Q

combined hormone therapy

A

treats menopausal symptoms, but increases density of breast tissue therefore complicating mammograms

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33
Q

long term estrogen+progestin use increases risk of breast carcinoma by what percent?

A

8%

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34
Q

long term use of just estrogen increases risk of breast carcinoma by what percent?

A

1%

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35
Q

mutant BRCA1 gene

A

increases breast cancer (80%) and ovarian carcinoma (20-40%) risk, large gene with many mutations

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36
Q

mutant BRCA2 gene

A

increases breast cancer (80%) and ovarian carcinoma (10-20%)

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37
Q

clinical manifestations of breast carcinoma

A
  • lump in breast
  • nipple or skin retraction
  • skin edema (orange peel sign, skin around nipple looks like an orange peel)
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38
Q

3 classification criteria of breast carcinoma

A
  1. site of origin (ductal, lobular, in situ)
  2. presence or absence of invasion
  3. degree of differentiation of tumor cells (well-normal tissue, poor-bizarre cells)
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39
Q

ductal carcinoma accounts for how many breast carcinomas?

A

90%

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40
Q

in situ cancer

A

non-invasive, can become invasive

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41
Q

mammogram can identify carcinoma up to how long before a manual breast exam?

A

2 years

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42
Q

modified radical mastectomy

A

aka total mastectomy with axillary lymph node dissection

  • resecting (removing) entire breast, axillary tissue with lymph nodes
  • can be followed by breast reconstruction
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43
Q

partial mastectomy

A

removing the part of the breast with the tumor

-axillary nodes removed, radiation follows to make sure all carcinoma is gone

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44
Q

lumpectomy

A

removing the tumor and a small amount of adjacent breast tissue, and the axillary nodes followed by radiation

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45
Q

adjuvant therapy

A

eradicate any tumor cells that may have spread beyond the breast

  • anticancer drugs (adjuvant chemo)
  • anti estrogen drugs (adjuvant hormonal therapy)
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46
Q

in adjuvant therapy, part of the tumor is surgically tested to:

A
  1. detect presence of estrogen and progesterone receptors

2. detect amplification of HER-2 gene that speeds growth rate of tumor cells (if positive, prognosis is worse)

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47
Q

hormone receptor status

A

if estrogen receptors (ER) and progesterone receptors (PR) are present in breast carcinoma, prognosis is more favorable
-treatment used is anti estrogen adjuvant therapy

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48
Q

recurrent and metastatic carcinoma

A
  • can appear many years after original tumor

- no longer curable and treatment is to control growth and improve quality of life

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49
Q

treatment for recurrent carcinoma

A

tumor is hormone receptor positive:
-use anti estrogen drugs in premenopausal
-use aromatase inhibitor drugs in postmenopausal
tumor is hormone receptor negative:
-hormonal manipulation
radiation controls deposits in bone

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50
Q

breast sarcoma

A

rare, arises from fibrous tissue or blood vessels

  • large and bulky
  • may metastasize widely
  • treatment is surgical resection (removal)
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51
Q

vaginitis

A

common, causes vaginal discharge, itching, and irritation

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52
Q

cervicitis

A

mild chronic inflammation, common in women that have had children
-can spread to infect tubes and adjacent tissues, causing pelvic inflammatory disease

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53
Q

salpingitis

A

tubal infection

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54
Q

pelvic inflammatory disease (PID)

A

inflammation of fallopian tubes, and sometimes the ovaries

-manifests as lower abdominal pain and tenderness, fever, and can cause tubal scarring

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55
Q

condylomas

A

venereal warts in genital tract

-tumor like overgrowths of squamous epithelium transmitted by sexual contact, benign

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56
Q

common locations of condylomas

A

mucosa of cervix and vagina, vaginal opening, anus

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57
Q

treatment of condylomas

A

aims to destroy the lesions

  • freezing
  • surgical excision
  • strong chemical
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58
Q

endometriosis

A

deposits of endometrial tissue outside normal location

  • uterine wall, ovary, elsewhere in pelvis, appendix, rectum
  • the tissue undergoes cyclic desquamation (shedding) causing intense cramping, can cause scarring
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59
Q

what diagnoses endometriosis

A

laparoscopy-visualization of ectopic deposits followed by removing or destroying the deposits

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60
Q

treatment of endometriosis

A
  • synthetic hormones-suppress menstrual cycle
  • oral contraceptives-suppress ovulation, retarding progression of endometriosis
  • drugs that suppress output of gonadotropin-declin in ovarian function, deposits of endometriosis regress
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61
Q

cervical polyps

A

benign, arise from cervix and usually small

-need to be surgically removed, erosion of the tip can cause bleeding

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62
Q

cervical dysplasia

A

abnormal growth and maturation of cervical squamous epithelium
-mild and severe dysplasia

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63
Q

mild cervical dysplasia

A

results from cervical dysplasia and regresses spontaneously

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64
Q

severe cervical dysplasia

A

does not regress and can progress to in situ carcinoma, which then may progress to invasive carcinoma

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65
Q

cervical intraepithelial neoplasia

A

different stages in a progressive spectrum of epithelial abnormalities with 3 grades
Grade I: mild
Grade II: moderate
Grade III: severe

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66
Q

HPV genital tract infection

A

80+ strains, 8 are carcinogenic

  • common in young sexually active women
  • 90% of infections resolve themselves in 6-12 months
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67
Q

diagnosis of HPV

A

pap smear with inconclusive results, HPV test given

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68
Q

HPV vaccine

A
  • 1st vaccine: 2006, protects types 6, 11, 16, and 18

- 2nd vaccine: 2009, protects types 16 and 18

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69
Q

types 6 and 11 are responsible for what?

A

90% of genital tract condyloma

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70
Q

types 16 and 18 are responsible for what?

A

70% of cervical dysplasia and carcinoma

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71
Q

cervical dysplasia and carcinoma

A

develops in cells between squamous epithelium at exterior cervix and columnar epithelium lining cervical canal (between exterior cervix and cervical canal)

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72
Q

treatment for cervical dysplasia and carcinoma

A

dysplasia and in situ: freezing, surgical excision, hysterectomy (produce excellent results)
invasive carcinoma: radiation, radical hysterectomy (les satisfactory results)

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73
Q

radical hysterectomy

A

resection (removal) of uterus, fallopian tubes, ovaries, and adjacent tissues

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74
Q

benign endometrial hyperplasia

A

irregular uterine bleeding

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75
Q

benign endometrial polyps

A

common, and may cause bleeding if tip is eroded

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76
Q

endometrial adenocarcinoma

A

prolonged endometrial stimulation by estrogen use, has irregular uterine bleeding or postmenopausal bleeding

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77
Q

uterine myoma

A

benign smooth muscle tumor from uterine wall

  • 30% women over 30 have them
  • cause irregular/heavy uterine bleeding
  • pressure on bladder and rectum
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78
Q

dysfunctional uterine bleeding

A

follicle fails to mature and no corpus luteum is formed, subjecting uterus to continuous estrogen stimulation so it sheds and bleeds in an irregular fashion instead of all at once

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79
Q

first part of menstrual cycle

A

endometrial glands and stroma proliferate under influence of estrogen

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80
Q

mid-cycle of menstrual cycle

A

ovulation-follicle discharges egg, become corpus luteum that produces estrogen and progesterone
-endometrium undergoes secretory phase, prepares to receive fertilized ovum

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81
Q

what happens if no pregnancy occurs

A

corpus luteum degrades, estrogen-progesterone levels fall, and secretory endometrium is shed with blood and a new cycle begins

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82
Q

dysmenorrhea

A

primary and secondary-painful periods, typically involving abdominal cramps

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83
Q

primary dysmenorrhea

A

most common, periods painless for first two years after menarche, then prostaglandins are synthesized under influence of progesterone and released from endometrium and cause pain

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84
Q

primary dysmenorrhea pain

A

crampy lower abdominal pain that begins just before menstruation, and lasts for 1-2 days after onset of menstrual flow
treatment: prostaglandin inhibitors and oral contraceptives

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85
Q

secondary dysmenorrhea

A

from diseases of pelvic organs, such as endometriosis

-treatment: correct the underlying disease

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86
Q

ovarian cysts

A

arise from ovarian follicles or corpora lute that have failed to regress normally and converted to fluid-filled cysts

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87
Q

functional cysts

A

follicle and corpus luteum cysts from deranged maturation and involution (shrink), regress spontaneously, don’t become large

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88
Q

endometrial cysts

A

endometrial deposits in ovary filled with old blood and debris

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89
Q

benign cystic teratoma

A
  • dermoid cyst
  • come from unfertilized ova that undergo neoplastic change
  • contain skin, hair, teeth, parts of GI tract, other tissues
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90
Q

malignant teratoma

A

very rare, usually benign

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91
Q

ovarian tumors

A

resemble epithelium found in other parts of genital tract

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92
Q

serous tumor

A

resembles cells lining fallopian tubes

  • cystadenoma
  • cystadenocarcinoma
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93
Q

cystadenoma

A

benign, cystic serous tumor

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94
Q

cystadenocarcinoma

A

neoplastic epithelium may extend on the surface of tumor and break off, implanting in other places

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95
Q

mucinous tumor

A

resembles mucus-secreting tumor of endocervix

  • mucinous cystadenoma
  • mucinous cystadenocarcinoma
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96
Q

endometrioid tumor

A

resembled endometrial tissue (endometrioid carcinoma)

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97
Q

fibroma

A

from fibrous connective tissue cells of ovary

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98
Q

granulosa

A

theca cell tumor

  • ovarian, produces estrogen
  • from granulose cells (estrogen producing cells) that line follicle
  • induces endometrial stimulation
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99
Q

male hormone-producing ovarian tumors

A

induces masculinization in a female

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100
Q

vulvar dystrophy

A
  • irregular white patches (leukoplakia) on vulvar skin
  • intense itching
  • can progress to carcinoma, local treatment is usually effective
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101
Q

carcinoma of the vulva

A
  • in both pre and post menopausal women
  • usually w/ preexisting vulvar dystrophy
  • treated by vulvectomy and excision of inguinal lymph nodes
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102
Q

toxic shock syndrome

A

most common in women that use high absorbency tampons

  • toxin produced by staphylococci
  • menstrual blood and secretions are a good culture medium
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103
Q

how do tampons cause toxic shock syndrome

A

they slow drainage of menstruate, may cause superficial erosions on vaginal mucosa allowing toxin to be absorbed

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104
Q

clinical manifestations of TSS

A

fever, vomiting, diarrhea, muscle pains, sunburn-like rash followed by flaking and peeling

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105
Q

treatment of TSS

A

general supportive measures, discontinue tampon use, antibiotics eradicate staphylococci but do not shorten course

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106
Q

what is recurrence rate of TSS?

A

30%

107
Q

natural family planning

A

avoidance of intercourse at the time of ovulation

108
Q

artificial contraception

A

barrier methods, oral contraceptives, intrauterine contraceptives

109
Q

barrier methods of contraception

A

diaphragms and condoms, effective, and no side effects

110
Q

oral contraceptives

A

suppress ovulation, but have side effects such as hypertension and increased risk for thromboembolus

111
Q

intrauterine contraceptive devices

A

prevent implantation, but increased incidence of tubal infection and tubal pregnancy

112
Q

emergency contraception

A

prevents pregnancy following unprotected intercourse or sexual assault
-within 12 hours: risk of pregnancy

113
Q

how long do sperm survive in genital tract?

A

6 days, can still fertilize an ovum

114
Q

fertilization

A

union of sperm and ovum in fallopian tube

  • ovum expelled from follicle at ovulation
  • first cell division completed 30 hrs. after fertilization
  • only 1 sperm
115
Q

trophoblast

A

cell that forms the placenta and membranes after fertilization occurs and zygote develops into small ball of cells

116
Q

implantation occurs by…?

A

the end of the 1st week

  • implants in endometrium, amniotic sac and yolk sac form
  • organ systems begin to form
117
Q

stages of prenatal development

A

pre-embryonic period, embryonic period, fetal period

118
Q

pre-embryonic period

A

3 weeks after fertilization

-blastocyst becomes implanted and inner mass cell differentiates into 3 germ layers

119
Q

embryonic period

A

3rd-7th week

  • assumes human shape
  • organ systems formed
  • critical development period
120
Q

fetal period

A

8th week to term

  • fetus continues to grow
  • no major structure changes
  • subcutaneous fat accumulates
121
Q

duration of pregnancy

A

time of conception: 38 weeks

from first day of last period: 40 weeks

122
Q

gestation

A

total duration of pregnancy from fertilization to delivery

123
Q

amniotic sac

A

enclosed within chorion, forms protective environment for fetus

124
Q

yolk sac

A

forms intestinal tract of fetus

125
Q

fetoplacental circulation

A

circulation from the fetus to the villi

126
Q

uteroplacental circulation

A

maternal blood circulates around villi

127
Q

functions of placenta

A
  • provide oxygen and nutrition

- synthesizes hormones (human chorionic gonadotropin HCG)

128
Q

amniotic fluid

A

produced by filtration and excretion of maternal blood and fetal urine

129
Q

polyhydramnios

A

increased volume of amniotic fluid

  • fetus can’t swallow it and it accumulates
  • or fluid is swallowed but not absorbed
130
Q

oligohydramnios

A

reduced volume of amniotic fluid

  • fetal kidneys failed to develop and no urine is formed (no excretion)
  • or congenital obstruction of urethra doesn’t allow urine to form amniotic fluid
131
Q

what causes “morning sickness?”

A

hormones produced by endocrine glands maintain the pregnancy
-sometimes estrogen increases too rapidly and causes nausea and vomiting that usually subsides by the end of the first trimester

132
Q

hyperemesis gravidarum

A

excessive vomiting, more prolonged and severe than normal

-it usually requires treatment if there is weight loss and dehydration present

133
Q

gestational diabetes

A

hyperglycemia (high blood sugar) is harmful to fetus

  • pregnancy hormones induce maternal insulin resistance, and insulin secretion cannot increase to compensate
  • usually relents after delivery, but increases change for type 2 diabetes later
134
Q

spontaneous abortion

A

10-20% of all pregnancies

  • early: from chromosome abnormalities, defective implantation, or maldevelopment
  • late: from placenta detachment, obstruction of blood supply, or drug abuse such as cocaine that disrupts blood flow to placenta
135
Q

ectopic pregnancy

A

development of embryo outside the uterine cavity, most commonly in the fallopian tubes

136
Q

predisposing factors to ectopic pregnancy

A

previous fallopian tube infection, failure of normal contractions of tubal wall, or both fallopian tubes predisposed

137
Q

consequences of ectopic pregnancy

A

fallopian tube rupture, bleeding from torn vessels, can be life threatening to the mother

138
Q

if oral contraceptives fail and are continually used, what can happen?

A

the developing embryo is exposed to synthetic estrogen and progestin compounds, which may induce congenital abnormalities in the fetus

139
Q

velamentous insertion

A

umbilical cord attaches to the fetal membrane instead of the placenta

  • may tear or be compressed during labor
  • can be fatal to the infant
140
Q

placenta previa

A

placenta attaches to the lower part of uterine wall instead of high

  • central and partial
  • causes episodes of bleeding
  • requires c section delivery
141
Q

central placenta previa

A

placenta covers entire cervical opening

142
Q

partial placenta previa

A

partially covers cervical opening

143
Q

3 disadvantages of having twins

A
  1. twins are smaller than a single infant at comparable gestational stage
  2. overdistention (over stretching) of uterus promotes premature delivery
  3. congenital malformations occur 2x as often
144
Q

twin transfusion syndrome

A

vascular anastomoses (joined blood vessel) connects placental circulation of identical twins

  • one is polycythemic (increased RBC), one is anemic
  • fatal if amount of blood is too disproportionate
145
Q

vanishing twin

A

one twin dies in the womb and is reabsorbed

146
Q

blighted twin

A

one twin dies in the womb and persists as a degenerated fetus

147
Q

fraternal twins

A

2 separate ova fertilized by 2 separate sperm, results in two babies born at the same time that don’t look alike

148
Q

identical twins

A

single ovum that splits into two ova, results in two babies born at the same time that look almost exactly alike

149
Q

conjoined twins

A

union between identical twins

150
Q

perinatal period

A

time period immediately before and after birth

151
Q

preeclampsia

A

high blood pressure and signs of organ damage in a pregnant women-condition that sometimes progresses to eclampsia

152
Q

symptoms of preeclampsia

A

proteinuria, feet/hand swelling, could have seizure or stroke causing decreased delivery of blood to the baby

153
Q

signs of preeclampsia

A

abdominal pain, persistent headache, high weight gain

154
Q

causes of preeclampsia

A

pregnant with twins or more, advanced maternal age, obesity, first pregnancy, history of hypertension

155
Q

when does preeclampsia start developing and when do signs/symptoms occur?

A

starts developing during 1st trimester, symptoms seen in 2nd trimester

156
Q

eclampsia

A

condition that follows preeclampsia

-marked by seizures in a pregnant woman

157
Q

symptoms of eclampsia

A

muscle aches, seizures, severe agitation, unconsciousness

-can cause organ failure and death

158
Q

high blood pressure and proteinuria of preeclampsia usually resolve within:

A

6 weeks

159
Q

diagnosis of preeclampsia

A

blood pressure greater than 140/90, and greater than 300mg of protein in urine

160
Q

previous preeclampsia brings what risk of getting hypertension again?

A

4x

161
Q

gestational trophoblast disease

A

trophoblastic cells covering the villi continue to grow at an excessive rate, producing higher human chorionic gonadotropin

  • tissue may invade uterus, vagina, etc
  • hydatidiform moles
162
Q

hydatidiform mole (fluid filled vesicle)

A

occurs in 80% of affected patients

  • complete, partial, invasive mole
  • abnormal fertilization of an ovum lacking chromosomes, fertilized by single sperm bearing X chromosome duplicated to form 46
163
Q

hydatidiform mole (complete)

A
  • both x chromosomes come from father
  • no embryo
  • villi become cystic structures resembling mass of grapes
164
Q

hydatidiform mole (partial)

A
  • normal ovum fertilized by 2 sperm, resulting in fertilized ovum with 3 sets of chromosomes (69)
  • embryo forms but does not survive
165
Q

invasive mole

A

occurs in gestational trophoblast disease

  • trophoblastic tissue invades deeply into the uterine wall
  • very aggressive, occurs in 15% of affected patients
166
Q

choriocarcinoma

A

arise following incomplete removal of invasive mole or incompletely removed mole

  • proliferating trophoblast may extend to vagina, metastasize to lungs and brain
  • treatment is hysterectomy and chemo
167
Q

erythroblastosis fetalis

A

mother is sensitized to an antigen in fetal RBCs, she forms antibodies against the antigen that cross the placenta, which damage the fetal RBCs. fetus will increase blood production to compensate

168
Q

hydrous fetalis

A

complication of erythroblastosis fetalis

-severe anemia (RBC deficiency) that causes heart failure, edema, death during last trimester

169
Q

less intense hemolytic process

A

complication of erythroblastosis fetalis

-infant is born alive but anemic (RBC deficient)

170
Q

mild disease

A

complication of erythroblastosis fetalis

-infant appears normal at birth, then becomes anemic and jaundiced and develops edema

171
Q

Rh hemolytic disease

A

the baby and the mother are either Rh-positive (contain the D antigen) or Rh-negative (don’t contain D antigen) but are not the same

  • usually RH negative mother, and RH positive baby, mother forms anti-D antibodies that cross placenta
  • normal in first pregnancy
172
Q

prevention of Rh hemolytic disease

A

Rh immune globulin

  • if administered within 72 hours after delivery, antibody coats Rh antigen sites on surface of fetal red cells in maternal circulation to reduce sensitization and development of antibodies
  • some drs recommend late preg. injections and after delivery
173
Q

ABO hemolytic disease

A

mother is type O (has anti-A and anti-B antibodies) while infant is type A or type B

  • maternal antibodies attach to fetal red cells
  • milder than RH hemolytic disease, A and B antigens are less developed
174
Q

ureter

A

conveys urine into bladder by peristalsis

175
Q

renal pelvis

A

expanded upper portion of ureter, inside of kidney

176
Q

major calyces

A

subdivision of renal pelvis

177
Q

minor calyces

A

subdivisions of major calyces into with renal papillae discharge

178
Q

bladder

A

stores urine

-discharge urine to urethra

179
Q

urethra

A

conveys urine from the bladder for excretion

180
Q

kidneys

A

produce urine

-divided into outer cortex and inner medulla

181
Q

3 basic functions of kidneys

A
  1. excrete waste products of food metabolism (CO2 and H2O, urea and other acids)
  2. regulate mineral and H2O balance
  3. produces erythropoietin and renin
182
Q

erythropoietin

A

specialized cells in the kidneys that regulate RBC production in bone marrow

183
Q

renin

A

specialized cells in the kidneys that regulate blood pressure

184
Q

nephron

A

basic structural and functional unit of the kidney

-made of glomerulus and renal tubule

185
Q

how many nephrons in one kidney?

A

about 1 million

186
Q

glomerulus

A

tuft of capillaries that filters the urine

187
Q

mesangial cells

A

phagocytic cells that hold the capillary tuft together and regulate the diameter of capillaries which affects filtration rate

188
Q

renal tubule

A

reabsorbs most of filtrate, secretes unwanted components into tubular fluid, regulates H2O balance

189
Q

proximal end of renal tubule is called..

A

Bowman’s capsule

190
Q

distal end of renal tubule is called…

A

Bundle of His-collecting tubules that the renal tubule empties into

191
Q

3 requirements for normal renal function

A
  1. free flow of blood through glomerular capillaries
  2. normally functioning glomerular filter
  3. normal outflow of urine
192
Q

angiotensin II

A

vasoconstrictor-raises blood pressure by causing peripheral arterioles to constrict

  • higher blood pressure, increased fluid in vascular system
  • stimulates aldosterone secretion from adrenal cortex which increases absorption of water by kidneys
193
Q

normal kidney development

A
  • kidneys arise from mesoderm, develop in pelvis, ascend to position
  • bladder derived from lower end of intestinal tract
  • excretory ducts develop from buds that extend from bladder into developing kidneys
194
Q

renal agenesis

A

failure of one of both kidneys to develop

  • bilateral: cannot live; rare
  • unilateral: common, other kidney enlarges to compensate
195
Q

duplications of urinary tract

A

complete duplication: formation of extra ureter and renal pelvis
incomplete duplication: only upper part of excretory system duplicates

196
Q

malposition

A

one or both kidneys, associated with:

  • kindey fusion
  • horseshoe kidney
  • fusion of upper pole of kidneys
197
Q

glomerulonephritis

A

inflammation of glomeruli caused by antigen-antibody reaction within glomerulus

  • failure to remove excess fluid, electrolytes, and waste from bloodstream
  • primary: occurs on its own
  • secondary: as a result of another disease
198
Q

signs and symptoms of glomerulonephritis

A
  • pink or cola colored urine from hematuria (RBC in urine)
  • foamy urine from proteinuria
  • hypertension
  • edema in face, hands, feet, and abdomen
  • fatigue from anemia or kidney failure
199
Q

what tests diagnose glomerulonephritis?

A

urinalysis, blood test (levels of waste in blood), imaging tests, kidney biopsy (determine cause of swelling)

200
Q

dialysis

A

artificial filtration when kidneys begin to fail

-peritoneal dialysis and extracorporeal dialysis

201
Q

peritoneal dialysis

A

-exchange of fluids across abdomen, can be done at home

202
Q

extracorporeal dialysis

A

filtration of waste products, must be done in a clinic attached to a machine up to a few times per week

203
Q

nephrotic syndrome

A

marked loss of protein in the urine-results from other diseases such as diabetes, lupus, other kidney diseases

  • excretion of protein > protein production
  • causes edema and ascites (fluid buildup in peritoneal cavity, causing abdominal swelling)
204
Q

prognosis of nephrotic syndrome in children vs. adults

A

children-minimal glomerular change, complete recovery

adults-manifestation of severe progressive renal disease

205
Q

arteriolar nephrosclerosis

A

complication of severe hypertension where renal arterioles thicken from carrying blood at a high pressure
-glomeruli and tubules degenerate, causing narrowing (reduced filtration, kidneys shrink, death from renal insufficiency)

206
Q

diabetic nephropathy

A

complication of long-standing diabetes

  • thickening of glomerular basement membranes
  • progressive impairment of renal function
  • can lead to nephrotic syndrome
  • can lead to renal failure, no treatment to slow progression
207
Q

gout-associated nephropathy

A

-elevated blood uric acid levels lead to increased uric acid, may collect in Henle’s loop and collecting tubules, causing tubular obstruction

208
Q

manifestation of gout-associated nephropathy

A

impaired renal function, which can lead to renal failure

209
Q

urinary tract infections

A

very common, can be acute or chronic

-mostly caused by gram negative bacteria that contaminate perianal and genital areas and ascend the urethra

210
Q

predisposing factors to UTI

A
  • condition that impairs free urine drainage
  • stagnation of urine, favors bacteria
  • catheter or instruments into the bladder
  • kidney stones injuring mucous, allowing bacteria to invade
211
Q

cystitis

A

affects the bladder, and more common in women because the urethra is shorter, and elderly men because enlarged prostate interferes with bladder emptying

212
Q

manifestations of cystitis

A
  • burning pain on urination
  • desire to urinate frequently
  • urine has bacteria and leukocytes
  • responds well to antibiotics, but can spread upward into renal pelvis and kidneys if not treated
213
Q

pyelonephritis

A

involvement of upper urinary tract from an ascending bladder infection, or an infection being carried to the kidneys from the bloodstream

214
Q

clinical manifestations of pyelonephritis

A
  • localized pain and tenderness over affected kidney
  • responds well to antibiotics
  • some cases become chronic and lead to kidney failure
215
Q

vesicoureteral reflux

A

urine back flows into the ureter during urination

-predisposes to UTI and pyelonephritis

216
Q

urinary calculi

A

stones that form anywhere in the urinary tract

217
Q

predisposing factors to urinary calculi

A
  • high concentration of salta in urine
  • UTIs reduce solubility of salts, so more UTIs predisposes to calculi
  • urinary tract obstruction: causes stagnation, promoting infection
218
Q

staghorn calculus

A

urinary stones that increase in size to form large branching structures that adopt to the shape of the renal pelvis and calyces

219
Q

renal colic

A

type of pain caused by small kidney stones that pass through the ureters-stones can also become impacted and need removal

220
Q

treatment of urinary calculi

A

cystoscopy-removes stones lodged in distal ureter

shock wave lithotripsy-breaks up stones in proximal ureter to be excreted

221
Q

urinary obstruction leads to what

A

progressive dilation of urinary tract, causing atrophy of kidneys, can cause stone formation or infection

222
Q

foreign bodies in urinary tract

A
  • usually inserted by the patient
  • can injure the bladder
  • predisposes to infection
  • removed by cystoscopy unless necessary to surgically open the bladder
223
Q

single renal cyst

A

not associated with impaired renal function, common

224
Q

multiple renal cysts

A

most common cause is congenital polycystic kidney disease, where the cysts enlarge and destroy renal tissue leading to early onset of renal failure (middle age)

225
Q

renal tumors

A

cortical tumor, transitional cell tumor

226
Q

cortical tumor

A

arise from epithelium of renal tubules

  • adenomas usually small and asymptomatic
  • carcinomas are more common
  • hematuria is often the first manifestation, metastasizes to the bloodstream
227
Q

transitional cell tumor

A

arises from transitional epithelium lining urinary tract

  • hematuria is usually first manifestation
  • low malignancy, good prognosis
  • from bladder epithelium
228
Q

nephroblastoma (Wilms tumor)

A

rare, highly malignant, affects infants and children

  • diagnosed by urinalysis, x ray and ultrasound, renal biopsy
  • treated by nephrectomy, chemo, radiation
229
Q

renal failure (uremia)

A

retention of excessive byproducts of protein metabolism

-acute or chronic

230
Q

acute renal failure

A
  • caused by tubular necrosis from impaired blood flow to kidneys, or effects of toxic drugs
  • renal function usually returns
231
Q

chronic renal failure

A

progressive, chronic kidney disease; 50% from chronic glomerulonephritis
-also from diabetic nephropathy, nephrosclerosis

232
Q

manifestations of renal failure

A
  • weakness, loss of appetite, vomiting
  • anemia
  • toxic manifestations from retained waste products
  • edema
  • hypertension
233
Q

treatment of renal failure

A

hemodialysis (peritoneal and extracorporeal) and treating the hypertension

234
Q

renal transplantation

A

kidney must be from close relative donor or cadaver, and must have as similar HLA antigens as possible

  • identical twins only have identical HLA antigens
  • immune defense will respond to foreign antigens and attempt to reject the kidney unless suppressed by drugs
  • 90% of transplanted kidneys survive for 5 years
235
Q

duct system to transport sperm from testes to urethra

A
  • starts at epididymis
  • continues as vas deferens
  • extends upward in spermatic cords
  • enter prosthetic urethra as ejaculatory ducts
  • urethra divided into long penile urethra and short prostatic urethra
236
Q

prostate

A

spherical gland that surrounds urethra just below bladder base
-secretes fluid with high concentration of an enzyme, discharged into urethra during ejaculation

237
Q

seminal fluid

A

secretions from seminal vesicles mixed with prostatic secretions

238
Q

prostate has inner group and outer group of glands

A

inner glands: surround urethra, give rise to benign hyperplasia
outer glands: bulk of prostatic glandular tissue, give rise to prostatic carcinoma

239
Q

benign prostatic hyperplasia

A
  • enlargement of prostate glands, common in elderly men
  • involves inner group of glands
  • obstructs outflow of urine
  • only significant if it obstructs neck of bladder leading to incomplete emptying or causes complete tract obstruction
240
Q

complications of benign prostatic hyperplasia

A

cystitis (inflammation of bladder), pyelonephritis (inflammation of kidneys and pelvis), calculi formation, hydronephrosis (distention (enlargement) of renal pelvis with urine due to obstruction)

241
Q

gold standard of treatment of benign prostatic hyperplasia

A

transurethral resection-part of the prostate is removed through the urethra with an instrument

242
Q

prostatitis

A

inflammation of the prostate

  • acute: acute inflammation from spread of infection from bladder or urethra
  • chronic: mild inflammation, common, and causes few symptoms
243
Q

gonorrhea

A

common STDs, inflammation can spread to urethra and rectal mucosa. obstruction of vasa may block sperm transport and cause sterility

244
Q

nongonococcal urethritis

A

caused by chlamydia, causing acute urethritis, very similar to gonorrhea

245
Q

carcinoma of the prostate

A

originates in outer group of prostate glands

  • common in elderly men, can be asymptomatic early on
  • urinary obstruction from narrowed bladder neck
  • infiltration of surrounding tissues
  • spreads to bones of spine and pelvis
  • slow growing, may take 10 years before it metastasizes or obstructs bladder
246
Q

acid phosphatase

A

substance secreted by normal prostatic cells and tumor cells that leaks into the bloodstream
-high levels of this substance detected in prostate cancer

247
Q

prostate-specific antigen PSA

A

secreted by prostatic cells, not specific to prostate cancer but also elevated in prostatic hyperplasia

248
Q

diagnosis of prostate cancer

A

digital rectal exam, PSA or acid phosphatase test, biopsy, ultrasound

249
Q

treatment of prostate cancer

A

radical prostatectomy and radiation, removal of testes if metastasizing has occurred

250
Q

radical prostatectomy

A

removal of small localized tumor, but can cause erectile dysfunction due to disruption of nerve supply to the penis

251
Q

cryptorchidism

A

testis does not descend normally into the scrotum

  • usually retained in the abdominal cavity or inguinal canal
  • germ cells are destroyed at normal body temperature, which is higher in the abdomen
  • testis must be surgically replaced in scrotum
252
Q

how long should it take testes to descend in newborns?

A

within 6 months after birth

-if not occurred by 1 year, should be surgically brought into the scrotum

253
Q

testicular torsion

A

abnormally attached testis, leading to twisting of spermatic cord

  • cuts off blood supply and leads to infarction unless promptly untwisted
  • surgically untwisting and anchoring of testis
254
Q

hydrocele

A

excess fluid accumulates in tunica vaginalis (area behind testis), treated by aspiration (draining) or resection (removal)

255
Q

varicocele

A

varicose veins in spermatic cord, usually involving the left side of the scrotum
-can impair fertility, and treatment only required if it causes discomfort or impairs fertility

256
Q

3 bodies of vascular erectile tissue in penis

A

two lateral bodies: corpora cavernosa
midline body: corpora spongiosum that surrounds urethra
-all surrounded by thick fibrous connective tissue capsule

257
Q

erectile dysfunction

A

inability to achieve and maintain an erection, common and frequency increases with age

258
Q

causes of erectile dysfunction

A
  • low testosterone
  • damage to nerves supplying penis
  • impaired blood supply to penis
  • stress, emotional factors
  • certain BP drugs
259
Q

how an erection occurs

A

penile arteries normally constricted

  • sexual arousal causes nitric oxide release, which causes relaxation of smooth muscle walls that allows penile arteries to dilate
  • pressure of blood in cavernous bodies must be high to close draining veins
  • blood must flow into the penis faster than it drains out
260
Q

carcinoma of testis

A

cancer of testis, treated by removal of testicle and associated structures and chemo

261
Q

seminoma

A

malignant neoplasm of semen-producing epithelium

262
Q

malignant teratoma

A

composed of several types of malignant tissues

263
Q

choriocarcinoma

A

arises from trophoblastic tissues in the uterus

264
Q

carcinoma of the penis

A
  • rare in circumcised males
  • secretions accumulating under foreskin may be carcinogenic
  • treatment: partial/complete amputation of penis and removal of inguinal lymph nodes

Intro to Disease (4 decks)

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