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Pathophysiology > Genitourinary System Disorders > Flashcards

Genitourinary System Disorders Flashcards

1
Q

What is cryptorchidism?

A

Undescended testes. One or both of the testicles fail to move down into the scrotal sac. Testes develop intra-abdominally in the fetus

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2
Q

When do testes usually descend into the scrotum through the inguinal canal?

A

7 to 9 months gestation

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3
Q

What are the consequences of cryptorchidism?

A

Infertility, malignancy, testicular torsion (10x increased risk), psychological effects of an empty scrotum.

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4
Q

What is hydrocele?

A

Fluid accumulates in the layers around the scrotum.

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5
Q

Hematocele

A

blood in the layers around the scrotum

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6
Q

Spermatocele

A

a cyst in the epididymis (might contain sperm)

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7
Q

Varicocele

A

Enlargement of the veins of the scrotum

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8
Q

Testicular torsion

A

Twisting of the spermatic cord that suspends the testis and the spermatic vessels that supply the testis with blood

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9
Q

Orchitis

A

An infection of the testes

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10
Q

Mumps virus

A

An infection that can spread to testes through the bloodstream or the lymphatics. Can also be caused by rubella, other viruses ad bacterial infections.

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11
Q

S/s of mumps virus

A

Sudden onset, painful enlargement of testes (usually one testicle). Urinary symptoms absent. Symptomatic for 7-10 days. Atrophy of testes may occur - impacting spermatogenesis.

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12
Q

Testicular cancer prevalence

A

Relatively rare, most common in 15-29 year olds. 5 year survival rate of 97%

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13
Q

Testicular cancer tx

A

Surgical removal of testes and spermatic cord plus radiation

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14
Q

Risk factors for testicular cancer

A

cryptorchidism, family hx, personal hx

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15
Q

Stage I classification for testicular cancer

A

tumor confined to testes, epididymis, or spermatic cord

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16
Q

Stage II classification testicular cancer

A

tumor spreads to retroperitoneal lymph nodes below the diaphragm

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17
Q

Stage III classification testicular cancer

A

metastases outside the retroperitoneal nodes or above the diaphragm

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18
Q

Generally, what is prostatitis?

A

inflammation or swelling of the prostate gland

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19
Q

acute bacterial prostatitis etiology

A

ascending urethral infection (E. coli)

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20
Q

acute bacterial prostatitis manifestations

A

fever, malaise, frequent/urgent urination, urethral discharge

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21
Q

acute bacterial prostatitis tx

A

antibiotics, reduce activity, hydration, pain management

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22
Q

chronic bacterial prostatitis

A

recurrent UTI, persistent in prostatic fluid and urine

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23
Q

What are the methods for retrieving different genitourinary specimens?

A

1st part of voided urine - urethral specimen. Midstream - bladder specimen. Prostatic expression obtained by prostatic massage, and urine after massage considered prostatic specimen.

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24
Q

Chronic bacterial prostatitis manifestations

A

Similar to acute - fever, malaise, frequent/urgent urination, urethral discharge

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25
Q

Tx for chronic bacterial prostatitis

A

Tx difficult: antibacterial drugs less effective in penetrating chronically inflamed prostate

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26
Q

Chronic prostatitis/chronic pelvic pain syndrome - inflammatory

A

Unknown cause. No bacteria, elevated leukocytes and abnormal inflammatory cells

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27
Q

Chronic prostatitis/chronic pelvic pain syndrome - noninflammatory prostatitis

A

symptoms resembling nonbacterial prostatitis. Negative urine cultures (normal leukocyte counts)

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28
Q

Benign Prostatic Hyperplasia (what is it)

A

age related, nonmalignant enlargement of the prostate gland

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29
Q

Characterization of BPH

A

formation of large discrete lesion in the periurethral region of the prostate, rather than peripheral zones (commonly affected by prostate cancer)

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30
Q

Static BPH stage

A

anatomical increase in prostatic size - result sin we urinary system, post void dribbling, frequency of urination, and nocturia

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31
Q

Dynamic stage BPH

A

Functional aspect of BPH - obstruction of urinary flow caused by enlarged prostate. When activated alpha 1 adrenergic receptors leads to smooth muscle constriction around prostate and urethra

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32
Q

Pathophysiology of BPH

A

Disruption in balance between testosterone, estrogen, and DHT (dihydrotestosterone). A relative increase in estrogen (with aging and decreased T) - sensitizes prostate to DHT = growth and enlargement

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33
Q

BPH Tx

A

alpha 1 adrenergic blocking drugs - relieves obstruction, increase urine flow (relaxes smooth muscle). 5 alpha reductase inhibitors (finasteride) - cause atrophy of prostate cells and block androgen effects of DHT. Surgery

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34
Q

Prostate Cancer prevalence

A

3rd to lung and colon/rectal cancer for cancer related deaths in Canadian males

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35
Q

Prostate cancer risk factors

A

Age (85% over age of 65). Diet and ethnicity. Diets low in veg and high in meat and saturated fats. Overweight and obese individuals. Androgens - increased levels

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36
Q

Screening for prostate cancer

A

Digital rectal exam

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37
Q

Diagnosis of prostate cancer

A

Biopsy, Gleason score, tumor markers (KLK3), MRI

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38
Q

Prostate cancer tx

A

Watchful waiting, surgery, radiation therapy, high intensity focused ultrasound, chemo, cryosurgery, hormonal therapy (antiandrogen), combination therapies

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39
Q

Prostate tumor grading -T1

A

primary stage tumors are asymptomatic and discovered on histologic examinations of prostatic tissue specimens

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40
Q

Prostate tumor grading system - T2

A

tumors are palpable on digital exam, but are confined to the prostate gland

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41
Q

Prostate tumor grading system - T3

A

tumors have extended beyond the prostate

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42
Q

prostate tumor grading system - T4

A

tumors have pushed beyond the prostate to involve adjacent structures

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43
Q

Vulva cancerous tissue

A

squamous cell carcinomas

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44
Q

Cervix cancer tissue

A

Squamous cell carcinomas, transformation zone

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45
Q

Endometrial cancer

A

associated with conditions producing excessive estrogen stimulation and endometrial hyperplasia

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46
Q

Ovarian Cancer

A

most common and most lethal cancer

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47
Q

Stage of Gynecologic cancer

A

0 - rarely used, preinvasive lesions; I - cancer is confined to organ it originated in; II - cancer involves some structures surrounding the organ of origination; III - regional spread of cancer with lymph node involvement; IV - distant spread of cancer with metastasis

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48
Q

Cervix Composition

A

undergoes functional changes during each menstrual cycle related to spermatozoa transport

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49
Q

Exocervix (visible portion) composition

A

stratified squamous epithelium (also lines vagina)

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50
Q

Endocervical canal composition

A

columnar epithelium

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51
Q

Varying composition of stratified squamous exocervix and mucus secreting endocervix

A

Periods of high estrogen production - cervix everts/turns outwards, columnar epithelium exposed to low vaginal pH -> metaplasia - gradual transformation from columnar to squamous. This dynamic area = transformation zone

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52
Q

transformation zone

A

critical area for development of cervical cancer. Vulnerable to dysplasia and susceptible to cancerous transformation. Transformation initially reversible, but can transform to carcinoma

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53
Q

Pap smear test focused area

A

transformation zone

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54
Q

Screening and Diagnosis of CErvical Cancer

A

Pap smear, colposcopy, cervicography, LEEP (loop electrosurgical excision procedure)

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55
Q

Tx of cervical cancer

A

Removal of lesion by one of following techniques: biopsy or local cautery; electrocautery, cryosurgery, or carbon dioxide laser therapy used to tx moderate to severe dysplasia limited to exocervix, radiation and surgery, radical hysterectomy, LEEP

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56
Q

Cervical cancer and STI

A

causal link between HPV infection and cervical cancer (increased with HPV subtypes 16, 18, also 31, 33, and 45

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57
Q

HPV med prevention

A

Gardasil or Cervarix vaccine prevents subtypes 16, 18, also 6 and 11

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58
Q

HPV subtypes responsible for 70% of cervical cancer

A

16 and 18

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59
Q

Two most common benign strains of HPV responsible for genital warts

A

6 and 11

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60
Q

Disorders of the Uterus - endometritis

A

cervical barrier is compromised,infection of the endometrium (the inner lining of the uterus

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61
Q

Disorders of the Uterus - endometriosis

A

Functional endometrial tissue is found in ectopic sites. Lesions stimulated by ovarian hormones, bleeding (pain) and pelvic adhesions

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62
Q

Disorders of the Uterus - endometrial cancer

A

most common cancer found in the female pelvis

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63
Q

Endometrial cancer types - Type 1

A

prolonged estrogen stimulation and endometrial hyperplasia. Hormone sensitive, low grade, favorable prognosis, painful bleeding

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64
Q

endometrial cancer types - benign

A

smooth muscle origin

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65
Q

endometrial cancer types - submucosal

A

displace endometrial tissue, more likely to cause bleeding, necrosis, and infection than other types

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66
Q

endometrial cancer types - subserosal

A

located beneath the perimetrium of the uterus

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67
Q

endometrial cancer types - intramural

A

embedded in the myometrium

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68
Q

Pelvic Inflammatory Disease (what is it)

A

inflammation of the upper reproductive tract that involves: the uterus (endometritis), fallopian tubes (salpingitis), the ovaries (oophoritis). A polymicrobial infection

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69
Q

Predisposing factors for pelvic inflammatory disease

A

16-24 years of age, nulliparity (never haven given birth), hx of multiple sexual partners, previous hx of PID

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70
Q

Complications of pelvic inflammatory disease

A

peritonitis, pelvic abscesses

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71
Q

What is an ectopic pregnancy

A

fertilized ovum implants outside uterus - most commonly in fallopian tube

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72
Q

Predisposing factors for ectopic prgenancy

A

pelvic inflammatory disease, therapeutic abortion, tubal ligation or tubal reversal, previous ectopic pregnancies, use of fertility drugs to induce ovulation

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73
Q

Ovarian Cysts

A

mot common form of ovarian tumor. Frequently cause menstrual and fertility problems. RElated to hypothalamic, pituitary, or adrenal dysfunction

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74
Q

Polycystic ovary syndrome (PCOS)

A

infertility, hyperandrogenism, common source of chronic anovulation, menstrual irregularity

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75
Q

Ovarian tumors

A

may be hormonally active: granulosa - excess estrogen production. Often diagnosed in advanced stage as many symptoms are nonspecific. May present with ascites. links to metastasis

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76
Q

Ovarian tumor tx

A

surgical excision

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77
Q

Majority of all ovarian malignancies

A

epithelial ovarian carcinomas arising from fallopian tube epithelium account for the majority

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78
Q

Screening for epithelial ovarian carcinomas

A

lack of effective screening strategies - emphasis on prevention

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79
Q

preventing epithelial ovarian carcinomas

A

removal of fallopian tubes(salpingectomy) if reproductive needs have been met

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80
Q

dysfunction of menstrual cycles - amenorrhea

A

absence of mensuration

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81
Q

dysfunction of menstrual cycles - hypomenorrhea

A

scanty mensuration

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82
Q

dysfunction of menstrual cycles - oligomenorrhea

A

infrequent menstruation (>35 days apart)

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83
Q

dysfunction of menstrual cycles - polymenorrhea

A

frequent menstruation (<21 days apart)

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84
Q

dysfunction of menstrual cycles - menorrhagia

A

excessive menstruation

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85
Q

dysfunction of menstrual cycles - metrorrhagia

A

bleeding between periods

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86
Q

dysfunction of menstrual cycles - menometrorrhagia

A

heavy bleeding during and between menstrual periods

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87
Q

Estrogen deprivation in menstrual cycle

A

retrogression of previously built up endometrium and bleeding. Bleeding is often irregular in amount and duration

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88
Q

Progesterone deprivation in menstrual cycle

A

abnormal menstrual bleeding (less). Absence allows estrogen to induce thicker endometrial layer with greater blood supply

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89
Q

menstrual cycle - dysmenorrhea

A

pain or discomfort with menstruation

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90
Q

primary dysmenorrhea

A

not associated with physical abnormality or pathology

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91
Q

secondary dysmenorrhea

A

organ condition exacerbated by the menstrual cycle: endometriosis, adenomyosis, pelvic adhesions, IUDS, PID- painful menstruation caused by organ abnormality

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92
Q

premenstrual syndrome - physical symptoms

A

painful and swollen breasts, bloating - abdo pain, headache and backache

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93
Q

premenstrual syndrome - psychological symptoms

A

depression, anxiety, irritability, behavioral changes

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94
Q

causes of symptoms of premenstrual syndrome

A

hyperprolactinemia, estrogen excess, alteration in estrogen - progesterone ratio, aldosterone,

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95
Q

disorders of the breast - mastitis

A

inflammation of the breast

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96
Q

disorders of the breast - fibroadenoma

A

firm rubbery, sharply defined round mass

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97
Q

disorders of the breast - fibrocystic

A

nodular granular breast masses

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98
Q

disorders of the breast - breast cancer

A

mass, puckering, nipple retraction, or unusual discharge

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99
Q

breast cancer prevalence

A

most common female cancer - 2nd leading cause of cancer relate deaths in women

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100
Q

breast cancer risk factors

A

Sex, age; hx of breast cancer or benign breast disease; hormonal influences; obesity; long term use of postmenopausal hormone therapy; alcohol; physical inactivity

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101
Q

Breast cancer screening

A

mammography (every 2 years from 50-74 years)

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102
Q

breast cancer known mutations

A

BRCA1 on chromosome 17 - tumor suppressor, BRCA2 on chromosome 13

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103
Q

Breast cancer diagnosis

A

physical examination, mammography, ultrasonography, percutaneous needle aspiration, stereotactic needle biopsy, excisional biopsy

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104
Q

STI portals of entry

A

mouth, genitalia, urinary meatus, rectum, skin

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105
Q

STIs can:

A

selectively infect the mucocutaneous tissues of the external genitalia, cause vaginitis, or produce genitourinary and systemic effects

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106
Q

HPV that results in genital warts

A

6 and 11

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107
Q

HPV that results in cervical dysplasia

A

16 and 18

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108
Q

HPV that results in cervical cancer

A

16 and 18

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109
Q

Neurotropic alpha group herpes viruses

A

Herpes simplex types 1 and 2, varicella zoster virus

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110
Q

Varicella zoster virus

A

shingles, chicken pox

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111
Q

Herpes simplex type 1

A

cold sores

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112
Q

Herpes simplex type 2

A

genital herpes

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113
Q

Lymphotropic beta group herpes viruses

A

cytomegalovirus, epstein-barr vius, human herpesvirus type 8

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114
Q

Pathogenesis of Genital Herpes infections

A

viruses replicate in the skin and mucous membranes at the site of infection (oropharynx or genitalia, grow in neurons and share biologic property of latency, virus ascends through the peripheral nerves to the sacral dorsal root ganglia

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115
Q

Diagnosis of genital herpes

A

based on symptoms, appearance of lesions, identification of the virus from cultures taken from lesions

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116
Q

Candidiasis

A

yeast like fungi, present in 20-50% of women without causing symptoms,

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117
Q

causes of Candidiasis

A

antibiotic therapy - suppresses the normal protective bacterial flora, high hormone levels owing to pregnancy, use of oral contraceptives - causes an increase in vaginal glycogen stores, diabetes mellitus or HIV infection - compromises immune system

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118
Q

Gonorrhea

A

a pyogenic gram-negative diplococcus that evokes inflammatory reactions characterize by purulent exudates (2nd most commonly reported STI in Canada

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119
Q

Gonorrhea hosts

A

human is the only natural host

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120
Q

gonorrhea host tissue

A

warm secreting epithelia

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121
Q

gonorrhea portal of entry

A

genitourinary tract, eyes, oropharynx, anorectum, or skin

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122
Q

Gonorrhea transmission

A

intercourse. May infect child in birth canal - risk of conjunctivitis and blindness if not treated in child

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123
Q

gonorrhea tx

A

tetracycline, penicillin, ceftriaxone, cefixime, ciprofloxacin, ofloxacin, etc

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124
Q

Chlamydia

A

most prevalent STI in Canada. 75% of females and 50% of males have no symptoms. Obligate intracellular bacterial pathogen. Chlamydia trachomatis - gram - negative bacteria

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125
Q

Chlamydia transmission

A

vaginal, anal, or oral sex. To child in birthing process

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126
Q

Chlamydia symptoms - female

A

mucopurulent vaginal discharge, pelvic pain, dysuria and hematuria, complications in 40% of cases - PIDc

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127
Q

Chlamydia symptoms - males

A

urethritis and purulent urethral discharge, testicular pain, prostatitis and epididymitis

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128
Q

chlamydia tx

A

azithromycin, doxycycline, amoxicillin (penicillin ineffective)

129
Q

Syphilis

A

bacterial spirochete - Treponeama pallidum. can spread to fetus in utero

130
Q

Syphilis complicaitons- birth

A

untreated congenital syphilis may result in prematurity, still birth, congenital defects and active infections

131
Q

Primary syphilis

A

appearance of chancre at the site of exposure

132
Q

secondary syphilis

A

last 1 week to 6 months. Symptoms of rash (esp palms and soles), fever, sore throat nausea, loss of appetite, and inflamed eyes

133
Q

tertiary syphilis

A

delayed response of the untreated disease - may be decades later

134
Q

tx of syphilis

A

penicillin

135
Q

Infection with HIV leads to immunodeficiency - why?

A

HIV primarily infects and destroys CD4 + T cells and other WBCs (CD8 + T cells, B cells and macrophages) - causing an inability of the immune to fight off infections

136
Q

HIV incorporates itself into host cells to replicate - which cells??

A

CD4 + T cells

137
Q

HIV in the cell

A

Usually DNA transcribes into RNA and that forms proteins. HIV takes RNA and reverse transcribe it into DNA of the host

138
Q

HIV complications

A

results in profound immunosuppression, develops in infections and cancers very readily, may advance to AIDS

139
Q

HIV transmission

A

semen can contain the virus, virus can be carried in blood, maternal - in utero, lactation, during labor and delivery

140
Q

Tests for HIV and AIDS

A

ELISA, saliva tests, viral load test, western blot, home tests

141
Q

Diagnosis of AIDS

A

less than 200 CD4 + T cells per cubic millimeter of blood, CD4+ T cells accounting for less than 14% of all lymphocytes, plus: one or more of a certain list of illnesses

142
Q

PrEP

A

prevents HIV

143
Q

PEP

A

taken within 72 hours of exposure to HIV

144
Q

ART

A

tx for HIV positive people to reduce levels in body

145
Q

HIV Tx

A

ART, cannot be cured

146
Q

Fx of Kidneys/Urinary System

A

filters blood (to produce urine), excretion of metabolic waste products and toxins, maintains fluid balance (regulates blood volume and BP), regulates solute concentration in body (osmolarity), maintains blood pH

147
Q

Kidney Structure and Location

A

multi-lobular structure, each lobule is composed of nephrons, the functional units of the kidney, located outside the peritoneal cavity in the back of upper abdomen, one on each side of the vertebral column at the level of the 12th thoracic to the 3rd lumbar vertebrae

148
Q

Nephron Functions - filtration

A

filtrate of blood pushes across glomerulus into the glomerular capsule (to form urine)

149
Q

Nephron Functions - reabsorption

A

movement of useful molecules from tubules back into blood (so they aren’t excreted in urine)

150
Q

Nephron fx - secretion

A

transport of undesirable molecules from blood into tubules

151
Q

Peritubular capillaries

A

located around PCT and DCT

152
Q

vasa recta

A

locate around loops of nephron

153
Q

Ureters

A

convey urine from kidney to bladder (1 ureter per kidney), lined in transitional epithelium; layer of smooth muscle

154
Q

urinary bladder

A

stores urine (500 mL - 1 L)

155
Q

Urethra

A

drains bladder, controls micturition

156
Q

2 urethral sphincters

A

internal (smooth muscle) - prevents leakage; external (skeletal muscle) - voluntary control

157
Q

Urine formation - output

A

output 1-2 L/dayby filtering blood

158
Q

Urine components

A

95% water, 5% solutes: electrolytes (Na, Cl, Mg, Ca, H, HCO3, PO4, K), urobilin, hormones, nitrogenous wastes: urea (protein breakdown), creatinine (creatine P breakdown), uric acid (nucleotide breakdown)

159
Q

Abnormal components of urine - glycosuria

A

glucose in urine - diabetes

160
Q

Abnormal components of urine - proteinuria

A

protein in urine - kidney disease/damage

161
Q

Abnormal components of urine - hematuria

A

blood cells/hemoglobin in urine - inflammation, infection, kidney stones, trauma

162
Q

Abnormal components of urine - bilirubinuria

A

bile pigments in urine - liver disease

163
Q

Abnormal components of urine - ketonuria

A

ketones in urine - starvation, diabetes low carb intake

164
Q

Tests for renal fx

A

GFR; urinalysis - specific gravity of urine, the high the number - the more dehydrated; blood tests - serum creatinine; blood urea nitrogen; cystoscopy, ultrasonography

165
Q

glomerular filtration

A

hydrostatic pressure in glomerular capillaries forces a filtrate of blood into glomerular capsule

166
Q

filtrate of blood components

A

water, electrolytes, nutrients (glucose, amino acids), urea, uric acid, creatinine

167
Q

What does filtrate not contain?

A

blood cells and proteins (too large to pass through)

168
Q

Glomerular Filtration Rate

A

volume of filtrate formed/minute. GFR affected by BP

169
Q

For filtration to occur…

A

glomerular hydrostatic pressure (GHP) > capsular hydrostatic pressure (CsHP) + blood colloid osmotic pressure (BCOP)

170
Q

Glomerular Hydrostatic PRessure

A

pressure exerted by blood in the glomerular capillaries

171
Q

capsular hydrostatic pressure

A

Pressure exerted by fluid in the capsule surrounding the glomerular capillaries in the renal corpuscle of the kidney.

172
Q

Blood colloid osmotic pressure

A

pressure exerted by proteins (primarily albumin) in the blood as it flows through glomerular capillaries

173
Q

What would happen if GHP was equal to CsHP + BCOP?

A

net filtration pressure would be 0 mm Hg = anuria (no urine formation)

174
Q

How is glomerular filtration regulated?

A

by regulating blood pressure and flow

175
Q

What is tubular reabsorption?

A

reabsorption of substances in filtrate back into blood (recovery of useful solutes)

176
Q

Where does most of the reabsorption in the nephron occur?

A

from the PCT (proximal convoluted tubule) because its cuboidal epithelium has microvilli - huge surface area

177
Q

What is reabsorbed into the blood by active transport?

A

Sodium (Na+) - 80% reabsorbed

178
Q

What is reabsorbed into the blood by facilitated transport and cotransport with Na+?

A

Glucose, amino acids, and vitamins (100% reabsorbed)

179
Q

What is reabsorbed into the blood in the nephron by diffusion?

A

Cl-, K+, Mg++, Ca++ (down electrochemical gradients) - 80% reabsorbed

180
Q

What is transported back into the blood by osmosis?

A

H2O (follows solute)

181
Q

Reabsorption (esp of water, Na+,and Cl-) also occurs along…?

A

nephron loop, DCT, and collecting duct

182
Q

Which hormone increase the calcium reabsorption from the DCT?

A

Parathyroid Hormone (PTH)

183
Q

Which hormone increases the reabsorption of Na+ from the DCT?

A

aldosterone -triggers synthesis of additional Na+/K+ transporters in the membrane of cells

184
Q

What does the reabsorption of HCO3- do?

A

Maintain blood pH by buffering H+ in blood

185
Q

What is the transport maximum (Tm)?

A

maximum transport for each substance (carriers get saturated) if renal threshold is exceeded, substances will appear in urine

186
Q

Tm for glucose?

A

375 mg glucose/min

187
Q

Where does tubular secretion occur?

A

along length of renal tubule

187
Q

Tubular Secretion

A

secretion of substances from peritubular blood into tubular filtrate (removal of undesirable solutes). Active transport of waste into filrate

188
Q

In tubular secretion where are H+, NH4+, and some drugs secreted?

A

PCT

189
Q

In tubular secretion, where is urea excreted?

A

nephron loop

190
Q

In tubular secretion, where is K+ secreted?

A

DCT

191
Q

An increase in aldosterone causes an increase in what?

A

K+ secretion (K+ secretion is coupled to Na+ reabsorption [Na+/K+countertransport)

192
Q

What is the fx of ADH?

A

makes collecting duct more permeable to H2O; water leaves and urine is concentrated

193
Q

Ascending loop of Henle

A

Thick, impermeable to water. NaCl actively transported out

194
Q

Descending loop of Henle

A

thin, water permeable

195
Q

Why is NaCl actively transported out of the ascending loop of Henle and not water?

A

To create a high concentration of solutes in the interstitial space surrounding the nephron that drives passive reabsorption of water into the interstitial space from the collecting ducts and the descending limb (fluid maintenance)

196
Q

Why does water leave the descending loop of HEnle?

A

due to the medullary gradient by NaCl being actively transported into the interstitial space by the ascending loop

197
Q

Loop diuretics action

A

exert effect in the thick ascending loop of henle

198
Q

Thiazide diuretics

A

prevent absorption of NaCl in the distal convoluted tubule

199
Q

aldosterone antagonists (potassium sparing diuretics)

A

reduce sodium reabsorption and decrease potassium secretion in late distal tubule and cortical collecting tubule site regulated by aldosterone

200
Q

What is erythropoietin?

A

Hormone excreted by the kidney in response to hypoxia - regulates the differentiation of RBCs in bone marrow

201
Q

What is the fx of vitamin D?

A

increases calcium reabsorption from the GI tract, excreted by kidneys, helps regulate calcium deposition in bone tissue

202
Q

What occurs when HCO3- combines with H+?

A

Carbonic acid is formed H2CO3

203
Q

What should the pH be?

A

7.35-7.45

204
Q

Volatile acid (H2CO3 - carbonic acid)

A

dissociates in H2O and CO2 and leaves via lungs

205
Q

nonvolatile acid or fixed acids

A

buffered by body proteins or extracellular buffers and are eliminated via kidneys. Product of metabolism of dietary proteins, oxidation of sulfur containing amino acids, etc, etc

206
Q

How is carbon dioxide transported in circulation?

A

dissolved as a gas, as a bicarbonate ion, as carbaminohemoglobin

207
Q

This reaction is catalyzed by carbonic anhydrase…

A

CO2 + H2O -> H2CO3 -> H+ + HCO3-

208
Q

How is pH regulated?

A
  1. Chemical buffer systems of the body fluids 2. the lungs (inc/decr ventilation, bicarbonate buffering system) 3. the kidneys which eliminate H+ and both reabsorb and generate HCO3-
209
Q

Where does most of H+ elimination (to maintain pH) and HCO3- reabsorption occur?

A

PCT - 80-90%

210
Q

LAb tests used in assessing acid-base balance

A
  1. arterial blood gases and pH 2. CO2 content and HCO3- levels 3. base excess or deficit 4. the anion gap
211
Q

What is the anion gap?

A

difference between the negatively charged and positively charged electrolytes. Anion gap high? - blood is more acidic

212
Q

Metabolic disorders

A

alteration in plasma bicarbonate due to changes in ECF acid-alkali levels (e.g. metabolic acidosis could result from renal bicarb wasting)

213
Q

respiratory disorders

A

alterations in PCO2 due to changes in alveolar ventilation rates (e.g. respiratory acidosis would result from impaired CO2 elimination)

214
Q

Metabolic Acidosis

A

A decrease in bicarbonate due to excessive production of metabolic acids, inability of kidneys to excrete acids, bicarbonate loss, increased plasma Cl- concentrations

215
Q

Respiratory compensation for metabolic acidosis

A

hyperventilation to decrease PCO2

216
Q

Renal compensation of metabolic acidosis

A

increased H+ excretion and increased HCO3- reabsorption

217
Q

Tx of metabolic acidosis

A

correct root cause, restore fluid and electrolyte loss, improve O2 delivery to overcome lactic acidosis, use of NaHCO3 under limited circumstances

218
Q

Metabolic alkalosis

A

increase in bicarbonate caused by excessive gain of bicarbonate or alkali, excessive loss of H+ ions, increased HCO3- retention, volume contraction

219
Q

Respiratory compensation of metabolic alkalosis

A

hypoventilation to increase PCO2

220
Q

Renal compensation of metabolic alkalosis

A

decreased H+ excretion and decreased HCO3- reabsorption

221
Q

Tx of metabolic alklalosis

A

KCL therapy - Cl- replaces HCO3- and K+ corrects potassium deficit allowing kidney to retain H+ while eliminating K+

222
Q

Metabolic alkalosis - vomiting

A

increase in pH due to primary excess of HCO3- ions caused by loss of H+ ions, net gain in HCO3, loss of Cl- ions in excess of HCO3- ions

223
Q

Respiratory acidosis

A

increase in the PCO2 due to acute or chronic conditions that impair effective alveolar ventilation and causes and accumulation of PCO2

224
Q

Renal compensation of respiratory acidosis

A

increased H+ excretion and increased HCO3- reabsorption

225
Q

Tx of respiratory acidosis

A

improve ventilation

226
Q

Respiratory alkalosis

A

decrease in PCO2 due to excessive ventilation (anxiety)

227
Q

renal compensation of respiratory alkalosis

A

decreased H+ excretion and decreased HCO3- reabsorption

228
Q

Tx of respiratory alkalosis

A

Correct underlying cause, supplemental O2 if hypoxic

229
Q

Most common renal congenital anomalies

A

anomalies in shape and position - e.g. horseshoe kidney - fusion of two kidneys

230
Q

What is dysgenesis?

A

failure of an organ to develop normally

231
Q

What is agenesis?

A

complete failure of an organ to developW

232
Q

What is Potter syndrome?

A

characteristic facial features of newborns with renal agenesis - eyes widely separated and have epicanthic folds, ears low set, nose borad and flat, chin receding. Causes: cystic renal dysplasia

233
Q

Hypoplasia

A

failure of an organ to reach normal size, normally only affects one kidney

234
Q

Cystic disease of the kidney

A

fluid filled sacs or segments of a dilated nephron

235
Q

What are the causes of cystic disease of the kidney?

A
  1. tubular obstructions that increase intratubular pressure 2. changes in the basement membrane of the renal tubules that predispose to cystic dilation 3. May be congenital, genetic, or result of a secondary pathology 4. replacement of kidney tissue by cysts reduces/removes functional properties
236
Q

Types of Cystic Disease of the Kidney

A
  1. Simple and acquired renal cysts 2. medullary cystic disease 3. polycystic kidney disease (PKD) - single gene disorders
237
Q

What are the polycystic kidney disease - autosomal dominant polycystic kidney disease, manifestations?

A

pain, gross hematuria, infected cysts, hypertension due to compression of intrarenal blood vessels

238
Q

What are the polycystic kidney disease - autosomal recessive polycystic kidney disease, manifestations?

A

bilateral flank masses, severe renal failure, impaired lung development, liver fibrosis, portal hypertension

239
Q

Causes of Urinary Tract Obstruction

A

Developmental defects, calculi (stones), pregnancy, BPH, scar tissue resulting from infection and inflammation, tumors, neurological disorders such as spinal cord injury

240
Q

Manifestations of Urinary Tract Obstruction depend on:

A

site of obstruction and cause, the rapidity with which the condition developed

241
Q

Common symptoms of Urinary Tract Obstructions

A

pain, s/s of UTI, manifestations of renal dysfunction

242
Q

What are the damaging effects of Urinary Obstruction?

A

hydronephrosis - urine filled dilation of renal pelvis and calices associated with progressive atrophy of kidneys due to obstruction of urine outflow

stasis of urine - predisposes to infection and stone formation

development of backpressure - interferes with renal blood flow and destroys kidney tissue (atrophy) while inducing formation of cysts

243
Q

Kidney Stones/Renal Calculi/Nephrolithiasis

A

crystalline structures that form from components of the urine

244
Q

Requirements for formation of kidney stones/renal calculi/nephrolithiasis?

A
  • a nidus to form
  • urinary environment that supports continued crystallization of stone components
  • high levels of circulating (for example) can become very concentrated in filtrate, under acidic conditions the filtrate will undergo precipitation of calcium and crystals will form
245
Q

Factors influencing the formation of renal calculi

A

-concentration of stone components in the urine
- the ability of stone components to complex and form stones
- the presence of substances that inhibit stone formation

246
Q

Types of renal calculi

A

-calcium stones (oxalate or phosphatase)
-uric acid stones
-cystine stones

247
Q

Examples of endogenous renal calculi inhibitors

A

Citrate (citric acid cycle by-product), magnesium, mucoproteins

248
Q

Prevention of Renal calculi

A

-dietary restriction (increase fluids, reduce Na+ to reduce Ca++ excretion, reduce animal protein)
-calcium salt supplementation
-thiazide diuretics (by decreasing saturation of calcium salts in urine)
-cellulose phosphatase

249
Q

Tx of Renal Calculi

A

-pain management
- antibiotic for infection
- removing stones - uteroscopic removal, percutaneous removal, extracorporeal lithotripsy (lasers)

250
Q

Dx of Renal Calculi

A

-urinalysis
-radiography
-intravenous pyelography
-ultrasonography

251
Q

UTIs prevalence

A

2nd most common type bacterial infection presenting in clinics after respiratory infections

252
Q

types of UTIs

A

-asymptomatic bacteriuria
-symptomatic infections
-lower UTIs - cystitis
-upper UTIs - pyelonephritis, more serious (ability to induce renal damage

253
Q

Causes of UTIs (uncomplicated)

A

bacteria that enter through the urethra
-E. coli (most common cause)
-non E. coli negative rods
-staphylococcus saprophyticus
-gram positive cocci

254
Q

Most common cause of gram-negative septicemia in hospitalized patients

A

catheter induced infection

255
Q

Causes of UTIs associated with stasis of urine flow

A

-anatomic obstructions (urinary tract stones, BPH, pregnancy, malformations of the uterovesical junction

-increased pressure resulting in reflux

-functional obstructions (neurogenic bladder, infrequent voiding, detrusor (bladder) muscle instability, constipation

256
Q

Body protective mechanisms against UTIs

A

-washout phenomenon - flushing out of bacteria through urine
-mucin layer (physical barrier)
-local immune responses
-normal flora of the vaginal periurethral area
-prostate secretions

alterations in pH, diet, and drug interactions can alter this normal production and result in infections

257
Q

Dx of UTIs

A

-based on symptoms and presence of microorganisms in urine
-xray fils, ultrasonography, and CT and renal scans are used to idenitfy contributing factors
-urine dipstick

258
Q

Tx of UTIs

A

-based on the pathogen causing the infection (C +S test)

259
Q

Characteristics of acute episode of Cystitis (bladder infection)

A

-frequency of urination (as often as every 20 mins)
-lower abdominal or back discomfort
-burning pain on urination (dysuria)
cloudy and foul smelling urine on occasion

260
Q

S/s of UTI

A

-urination urgency
-frequent urination
-painful urination (dysuria)
-hematuria
-cloudy or foul smelling urine
-pelvic discomfort/pressure
-low grade fever

261
Q

Urinary incontinence

A

involuntary voiding, many different causes

262
Q

Types of Urinary Incontinence

A

-Neurogenic incontinence - caused by nerve spinal cord or brain damage

-stress incontinence - leakage of urine with sudden pressure on the bladder and urethra

-overflow incontinence - weak bladder muscle or blockage, incomplete emptying

-urge incontinence/overactive bladder - condition where the bladder can no longer urinate normally

  • functional incontinence - physical barriers that block access to bathroom
263
Q

Tx for Urinary Incontinence

A
  • behavioral - manage fluid intake before bed

-drugs - alpha adrenergic agonists

-catheters and urine collecting devices

-surgery

264
Q

Immune Mechanisms of Glomerulonephritis

A
  • glomerular antibodies - inflammatory response - interact with antigens present in basement membrane of glomerulus

-circulating antigen-antibody complexes - can stimulate autoantibody reactions against the glomerular membrane or circulating complexes can get stuck in the glomerular filtration pore - immune and inflammatory damage to membrane

265
Q

Characteristics of Glomerulonephritis

A

-hematuria with red cell casts (clusters of RBCs held together by protein matrix derived from renal tubules

  • a diminished GFR
  • oliguria

-HTN

266
Q

Causes of Glomerulonephritis

A

-disease that provoke a proliferative inflammatory response of the endothelial, mesangial, or epithelial cells of the glomeruli
-inflammatory process: damages the capillary wall, permits RBCs to escape into the urine, produce hemodynamic changes that decrease the GFR

267
Q

Cellular changes in glomerular disease - Proliferative

A
  • endothelial
    -mesangial
    -leukocyte infiltration
    -crescent formation

disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage

268
Q

Cellular changes in glomerular disease - Basement membrane thickening

A

deposition of dense non-cellular material on endothelial and epithelial sides of basement membrane or within membrane

disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage

269
Q

Cellular changes in glomerular disease - sclerosis

A

increased extracellular material in mesangial , subendothelial or subepithelial tissue of the glomerulus

disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage

270
Q

Cellular changes in glomerular disease - fibrosis

A

deposition of collagen fibers

disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage

271
Q

Diffuse glomerular changes

A

involving all glomeruli/all parts

272
Q

focal glomerular changes

A

only some glomeruli affected

273
Q

segmental glomerular changes

A

only certain segment of glomeruli affected

274
Q

mesangial glomerular changes

A

only affects mesangial cells

275
Q

Urinary Changes in Glomerulonephritis

A

-proteinuria
-hematuria
-pyuria (increased WBCs)
-oliguria (low urine output)
-edema
-hypertension
-azotemia (buildup of nitrogenous products in the blood)

276
Q

Types of Glomerular Disease

A

-acute proliferative glomerulonephritis - immune complex mediated, induces inflammation, cells lost (RBCs and WBCs) and proteins, pyuria, hematuria, oliguria, low GFR HTN, granular casts

-rapidly progressive glomerulonephritis

-nephrotic syndrome - results from increased glomerular permeabilityy and loss of plasma proteins (albumin) in urine

-membranous glomerulonephritis

-chronic glomerulonephritis

277
Q

Nephritic syndrome vs nephrotic syndrome

A

nephritic syndrome - a disease
nephrotic syndrome - a collection of symptoms

278
Q

Nephritic syndrome(a disease) causes:

A

-strep throat
-lupus
-hereditary
-goodpasture syndrome
-reactions to meds
-too little K+
-too much Ca ++
-autoimmune diseases

279
Q

Diagnostic Features of Nephritic Syndrome (disease)

A

hematuria, mild to moderate proteinuria, HTN, oliguria, red casts in urine

280
Q

Clinical features of Nephritic syndrome (disease)

A

hematuria, edema (less than in nephrotic), oliguria, pruritus

281
Q

Nephrotic Syndrome (collection of symptoms) caused by:

A

-diseases and conditions that only affect the kidneys (focal segmental glomerulosclerosis)
-less commonly venous thromboembolism, ARF, or serious bacterial infection

282
Q

Diagnostic Features of nephrotic syndrome (collection of symtpoms:

A

-proteinuria
-hypoalbuminemia
-diagnosed based on these findings

283
Q

Clinical features of nephrotic syndrome

A

-edema
-hyperlipidemia
-hypercoagulability
frothy urine

284
Q

Tubulointerstitial disorders

A

-damage to the proximal loop, or distal portion of the nephron
-acute tubular necrosis

285
Q

What is renal tubular acidosis

A

-proximal tubular disorders that affect bicarbonate reabsorption

-damage to the proximal tubule is due to decreased bicarbonate, thus less H+

-H+ accumulates over and above any buffering that may be present from bicarbonate

286
Q

What is pyelonephritis

A

-inflammatory reactions will damage the tubular portion of the nephron resulting in decreased functioning

-underlying stimulus is the infective organism

-Tx must be aimed at removing the infective organism in order to lessen the inflammatory damage

287
Q

major groups of renal cancer

A
  • embryonic kidney tumors occurring during childhood

-adult kidney cancers

288
Q

Embryonic kidney tumor occurring during childhood

A

-Wilms Tumor
-onset - 3-5 years in one or both kidneys
-WT1 mutation on chromosome 11
-distorts the kidney and decreases its function
-surgery and chemo and radiation
-90-95% long term survival for stages 1-3

289
Q

Adult kidney cancers

A

-renal cell carcinomas
-silent disorder in early stages - symptoms indicate advanced disease
-triad S/s - hematuria, flank pain, prsence of palpable mass

290
Q

Renal failure

A

kidneys fail to remove metabolic end products from the blood and regulate the fluid, electrolyte, and pH balance of the extracellular fluids

291
Q

Acute renal failure (ARF)

A

-abrupt in onset

-often reversible if caught early and tx

292
Q

Chronic Kidney disease (CKD)

A

-end result of irreparable damage to kidneys

-develops slowly, usually over the course of a number of years

293
Q

Underlying causes of renal failure

A

-renal disease

-systemic disease

-urologic defects of non-renal origin

294
Q

Prerenal causes of ARF/AKI

A

-hypovolemia
-decreased vascular filling
-HF and cardiogenic shock
-decreased renal perfusion due to vasoactive mediators, drugs, diagnostic agents

results in decreased GFR - lack of flow to the kidney

295
Q

Postrenal causes of AKI/ARF

A

-bilateral ureteral obstruction

-bladder outlet obstruction

results in decreased GFR - result of backpressure on the kidney

296
Q

Intrinsic or Intrarenal causes of ARF/AKI

A

acute tubular necrosis (ATN) due to:
- prolonged renal ischemia

  • exposure to nephrotoxic drugs, metals, organic solvents

-trauma, burns and mjor surgery are common precursors

-intratubular obstruction resulting from hemoglobinuria (Hgb in urine), myoglobinuria, myeloma light chans or uric acid casts

-acute renal disease

297
Q

Phases of Acute renal failure

A

-onset or initiating phase - last hrs to days, time from onset of precipitating event until tubular injury occurs

-maintenance phase - chracterized by a marked decrease in GFR

-recovery phase - period during which repair of renal tissue takes places

298
Q

Common Causes of CKD

A

-HTN
-diabetes mellitus
-polycystic kidney disease
-cancers
-glomerulonephritis
-obstructions of the urinary tract
-diseases of the heart and lungs
-chronic use of pain medication

slow to develop and arising from other disorders, renal tissue slowly damaged and lost insidious onset

299
Q

Stages of CKD progression

A

-diminished renal reserve

-renal insufficiency

-renal failure

-end stage renal disease (ESRD)

300
Q

Clinical manifestations of CKD

A

-accumulation of nitrogenous wastes (azotemia)
-alterations in water, electrolyte, and acid base balance
-mineral and skeletal disorders
-HTN and alterations in cardiovascular fx
-gastrointestinal disorders
-neurologic complications
-disorders of skin integrity
-immunologic disorders

301
Q

Factors determining the manifestations of renal failure

A

-extent of renal function that is present

-coexisting disease conditions

-type of renal replacement therapy that the person is receiving

302
Q

CKD manifestations - accumulation o nitrogenous wastes (azotemia)

A

-urea starts to accumulate in blood (early sign of kidney failure) - can eventually result in uremia

-nitrogenous waste accumulation can occur in blood without symptoms (azotemia)

-uremia = symptoms associated with decreased clearance of nitrogenous wastes (when approx 2/3 of nephrons destroyed, encephalopathy, peripheral neuropathies, pruritus + serositis

303
Q

CKD manifestations - disorders of water, electrolyte, and acid base balance

A

-sodium water balance - early sign of kidney damage is polyuria with nearly isotonic urine to plasma, fluid volume expansion, edema, and HTN

-potassium balance - approx 90% of potassium excretion is through kidneys, excretion increases as kidney adapts to a decrease in GFR, hyperkalemia in late stage/renal failure

-acid base balance - kidneys normally regulate blood pH by eliminating hydrogen ions produced in metabolic processes and regenerating bicarb - breakdown can result in metabolic acidosis - can become stabilized with buffering capacity of bone - result in skeletal disorders due to increased bone resorption

304
Q

CKD manifestations - skeletal disorders

A

-decreased phosphate excretion and increased serum phosphate levels

-serum calcium levels decrease

-PTH is stimulated to increase bone resorption releasing calcium

-PTH increases phosphate excretion

-vit d synthesis is impaired (conversion to active form of vitamin d - calcitriol - occurs at kidney

-combo of these factors result in renal osteodystrophy

305
Q

2 major types of osteodystrophy

A

-high bone turnover
-low bone turnover

306
Q

Hematologic Disorders Accompanying renal failure - anemia

A
  • kidneys primary site for EPO production
  • iron deficiency - dietary restrictions and blood loss with dialysis
  • decreased blood viscosityand compensatory HR increase - angina linked to reduced O2 supply
    -hypoxic/oxidative stress at kidney may further contribute to CKD progressionH
307
Q

Hematologic Disorders Accompanying Renal Failure - coagulopathies

A

platelet function is impaired with CKD

308
Q

Cardiovascular disorders accompanying renal failure

A

-HTN - increased vascular volume, elevated peripheral vascular resistance; decreased renal vasodilator prostaglandins; increased RAAS system

-heart disease - left ventricular hypertrophy and dysfunction; ischemic heart disease

-pericarditis - approx 20% of people receiving chornic dialysis; metabolic toxins either from uremic state or dialysis

309
Q

CKD altered drug reabsorption

A

due to antacid treatment (contain phosphate, magnesium)

310
Q

CKD altered metabolism

A

-less protein bound drugs - man ydrugs bind to albumin, unbound drugs free to be metabolized

-alterations in dosage may be required qith CKD

-because of a loss of proteins (hypoalbuminemia)

311
Q

Tx during renal insufficiency stage of renal failure

A

-tx UTIs promptly
-avoid med with renal damaging potential
-control BP
-control blood glucose
-stop smoking

-dietary management - protein, carbs, fats, calories, potassium, sodium and fluid intake

312
Q

Med management of renal failure - hemodialysis

A

-artificial kidney - capillary tubes with semipermeable membranes

-typically requires 3 times/week 3-4 hrs

313
Q

Med management of renal failure - peritoneal dialysis

A

sterile dialyzing solution is injected into peritoneal cavity - metabolic end products and ECF diffuse into dialysis solution, remove after few hours, can be performed at home

314
Q

med management of renal failure - transplantation, sucess depends on

A

-health of recepient
-degree of histocompatibility
-organ preservation
-immunologic management
-organ rejection primary concern
-recipient must be on immunosuppressant therapy for rest of life

315
Q

CKD children causes

A

-congenital malformations
-inherited disorders
-acquired diseases
-metabolic syndromesMAnif

316
Q

manifestations of CKD in children

A

-severe growth impairment
-developmental delay
-delay in sexual maturation
-bone abnormalities
-developmental psychosocial problems

317
Q

CKD in elderly

A

-normal decrease in GFR with age
-increased detrimental effects of nephrotoxic drugs
-greater incidence of cerbrovascular, cardiovascular, and skeltal system effects
-

Pathophysiology (1 decks)

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