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Reproductive > Sweaty has 2 many lectures: CA, BPH, overactive bladder > Flashcards

Sweaty has 2 many lectures: CA, BPH, overactive bladder Flashcards

1
Q

anastrozole

A

aromatase inhibitor: REVERSIBLE (non-steroidal)

Tx: breast CA

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2
Q

exemestane

A

aromatase inhibitor: IRREVERSIBLE (steroid structure)

Tx: breast CA

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3
Q

letrozole

A

aromatase inhibitor: REVERSIBLE (non-steroidal)

Tx: breast CA

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4
Q

aromatase inhibitors

A

oral daily
block CYP19A1 mediated production of estrone and estradiol
Tx: ER+ breast CA in POST-menopausal (can’t use in pre-menopausal women: E comes from other mechanisms)
AE: post menopausal (hot flash, hair thinning), teratogen, arthralgia, diarrhea

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5
Q

raloxifene

A 
monthly IM
SERM
ER agonist: bone
ER antagonist: breast, uterus
Tx: ER+ breast CA
prevent: BRCA2 related breast CA
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6
Q

tamoxifen

A 
daily PO
SERM
metabolized via CYP2D6 to more potent products: possible sub-optimal effect in poor metabolizers (no FDA requirement for testing)
ER agonist: bone, uterus
ER antagonist: breast
Tx: ER+ breast CA
prevent: BRCA2 related breast CA 
BBW: endometrial CA/hypertrophy, vaginal bleeding
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7
Q

toremifene

A 
PO daily
SERM (derivative of tamoxifen)
CYP3A4 metabolism
Tx: ER+ breast CA 
BBW: QT PROLONGATION
lacks BBW of other SERM: but avoid with Hx of endometrial CA/hyperplasia and thromboembolic disease
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8
Q

fulvestrant

A

monthly IM
SERD: binds ER and prevents dimerization in the nucleus (pure antagonist)
Tx: ER+ breast CA
AE: post menopausal symptoms

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9
Q

SERM

A

selective estrogen receptor modifier
ER agonist MOA: recruits coactivators
ER antagonist MOA: recruits corepressors (HISTONE DEACETYLASE I stabilizes nucleosome and prevents mRNA production)
Tx: ER+ breast CA (more important in post menopause, but can use in pre)
prevent: BRCA2 breast CA (BRCA1 is ER-)
improves: lipid profile, increase bone mineralization
AE: teratogen, retinal degeneration
BBW: thromboembolic disease, stroke

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10
Q

goserelin

A

SC
GnRH agonist
Tx: breast CA, prostate CA

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11
Q

GnRH agonist in Tx of CA

A

use is CONTINUOUS: down regulates GnRH receptors causing fall of FSH and LH and therefore estrogen
FLARE UP of disease initially: bone pain (metastases), hypercalcemia, breast enlargement/tenderness
WEEKS to lower estrogen/androgen levels: use ANDROGEN RECEPTOR BLOCKERS until then
Tx: prostate CA, breast CA in PRE-menopausal women (not effective because ovaries aren’t working anyway)
AE: post-menopausal (including done density); decrease bone density, elevated lipids, weight gain, DM, CV risk, sexual dysfunction/ loss of libido, gynecomastia, injection site reaction
CI: PREGNANCY

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12
Q

pertuzumab

A

Her-2/neu Ab: blocks heterodimerization of HER2 with HER3/4 (EGFRs)
Tx: breast CA
AE: decreased left ventricular ejection fraction, neutropenia, leukopenia

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13
Q

trastuzumab

A

Her-2/neu Ab: binds juxtraglomerular region of extracellular domain of HER2
Tx: breast CA
AE: cardiac, renal, hepatic, pulmonary
BBW: cardiomyopathy, infusion rxn (respiratory)

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14
Q

ado-trastuzumab/ emtasine (T-DM1)

A

Her-2/neu Ab: binds receptor causing it to be internalized allowing linked chemo agent to act on microtubules
Tx: breast CA
BBW: HF/ventricular dysfunction, hepatic

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15
Q

her-2/neu mAb

A

IV
Tx: breast CA
AE: hypersensitivity (asthenia, faitugue, GI), blood dyscrasia, INFUSION RXN (dyspnea, hypotension, rash)
BBW: pregnancy

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16
Q

lapatinib

A

oral
TKI: inhibits HER1/2: binds INTRACELLULAR ErbB1/2 at ATP binding site preventing phosphorylation/activation of receptor
metabolism: CYP3A4/5
Tx: breast CA
AE: GI toxicity, hand-foot syndrome, rash, anemia/thrombocytopenia, QT PROLONGATION, LUNG (interstitial lung disease/pneumonitis)
BBW: CI in LIVER DISEASE (increase drug levels)
monitor: LFT

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17
Q

everolimus

A 
mTOR inhibitor: bind FKBP-12
substrate/inhibit: CYP3A4, P-gp
inhibits: CYP2D6
Tx: ER+ breast CA
AE: blood dyscrasia, hyperglycemia/lipidemia, elevated creatinine, diarrhea/constipation
monitor: blood glucose, CBC, LFTs, lipid-triglyceride-creatinine profiles
BBW: INFECTION, NEOPLASIA (lymphoma/SCC)
use with: EXEMESTANE
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18
Q

SERDs

A

selective estrogen receptor downregulator
Tx: ER+ breast CA (more important in post menopause, but can use in pre)
AE: post menopausal (hot flashes, asthenia, pain)

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19
Q

Why might the initial response to anti-estrogen treatment of breast CA not be sustained longterm?

A

SERM, SERD, aromatase inhibitors

CA finds alternative proliferation pathways

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20
Q

CYP3A4

A

tormifene
lapatinib (also 3A5)
everolimus

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21
Q

CYP2D6

A

tamoxien

everolimus

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22
Q

CYP19A1

A

aromatase inhibitors

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23
Q

What provides superior outcomes in postmenopausal women with breast CA compared to tamoxifen alone?

A

aromatase inhibitor for 5 years

or following tamoxifen up with aromatase inhibitors for 5 years total

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24
Q

P-gp

A

everolimus

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25
Q

How is triple neg. breast CA treated?

A

Sx (first for all breast CA)
drug therapy depends on tumor size, lymph involvement
adjuvant/neoadjuvant/metastatic: radiation, conventional chemo drugs

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26
Q

Besides determining drug choice for a patient, what is tumor genotyping used for?

A

determining prognosis: need for drug therapy after Sx?
good prognostic indicators: watch and wait
bad prognostic indicators: adjunctive therapy

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27
Q

standard adjuvant chemotherapy regimens for breast CA

A

ALL include cyclophosphamide and doxorubicin (with/out: taxol or fluorouracil)
exception: docetaxel and cyclophosphamide with or without doxorubicin

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28
Q

doxorubicin

A

anthracycline
MOA: intercalator, free radical generation, topo II inhibitor
Tx: triple neg. breast CA, ovarian CA, bladder CA
AE: CUMULATIVE CARDIOTOXICITY, secondary malignancy, myelosuppression, hepatic, extravasational necrosis

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29
Q

cyclophosphamide

A

Tx: triple neg. breast CA, ovarian CA
AE: renal, pulmonary fibrosis, secondary malignancy, blood dyscrasia

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30
Q

fluorouracil

A

Tx: triple neg. breast CA

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31
Q

Do PR+ tumors have a poor/good prognosis?

Why?

A

good
suppresses tumor invasion and metastasis by maintaining epithelial cell phenotype and impeding the EMT (epithelial-mesenchymal transition)

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32
Q

medroxyprogesterone

A

depo progestin
MOA: bind progestin receptors and block GnRH release
Tx: endometrial CA
AE: amenorrhea, edema, anorexia, weakness

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33
Q

megestrol

A

oral progestin
MOA: suppresses LH release, enhances estrogen degradation
Tx: endometrial CA
AE: weight gain, post menopausal, tumor flare, thrombophlebitis, thromboembolism, PE

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34
Q

docetaxel

A

taxol

Tx: triple neg. breast CA, prostate CA

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35
Q

carboplatin

A

platinum: less potent
Tx: ovarian CA, testicular CA
AE: MYELOSUPPRESSION: THROMBOCYTOPENIA, cumulative anemia, blood dyscrasia

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36
Q

cisplatin

A

MOA: platinum plus CCDP: ace on mitochondria to produce oxidative and reticular stress: cascade including pro-apoptotic BAK and BAX and VDAC; activates p53
platinum
Tx: ovarian CA, bladder CA, testicular CA
AE (actively pumped into these cells: OCT2): NEPHROTOXIC, OTOTOXIC, neuro
nephro: HYDRATE, AMIFOSTINE
oto: antioxidants
CDDP important for loss of activity

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37
Q

paclitaxel

A

taxol
Tx: ovarian CA, testicular CA
AE: MYELOSUPPRESSION

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38
Q

bacillus calmette-guerin (BCG)

A

intravesical instillation after TURBC
MOA: req. host immune response: binds urothelial cells and activates APCs to induce effector cells (CTLs, NKs, LAKs (lymphokine activated killer), BAKs (BCG activated killer) cells)
response in hours and lasts for days
Tx: bladder CA

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39
Q

mitomycin C

A

intravesical instillation
MOA: mono/bi-functional alkylating agent
Tx: bladder CA
AE: chemical CYSTITIS, contact DERMATITIS (PALMAR/PLANTAR ERYTHEMA); pancytopenia (if used IV), dyspnea/unproductive cough

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40
Q

thiotepa

A

intravescular instillation
MOA: polyfunctional alkylator with loss of aziridine (alkylator) moiety
small, lipophilic: easily penetrates urothelium: SYSTEMIC TOXICITY
Tx: bladder CA
AE: dysuria, urinary renetion, chemical/hemorrhagic CYSTITIS, RENAL dysfunction; pancytopenia (if used IV)

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41
Q

Tx of ovarian CA

  1. stage 1/2?
  2. stage 3/4?
  3. advanced?
  4. locally confined?
A

only conventional chemo (after Sx)

  1. stage 1/2: platinum drug with cyclophosphamide and/or doxorubicin
  2. stage 3/4: platinum drug with paclitaxel
  3. advanced: drugs given systemically
  4. local: option of intra-peritoneal instillation of cisplatin (1-2L, rotate side to side for coverage of peritoneal surface, then drained off)
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42
Q

Tx of bladder CA

  1. superficial disease
  2. with tumor progression
A
  1. trans-urethral resection of bladder CA (TURBC) followed by intravesical instillation (BCG, mitomycin, thiotepa)
  2. conventional chemo, csytectomy
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43
Q

platinum drugs

A

DNA intrastrand crosslinks: N7

AE: allergy, myelo-suppression

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44
Q

taxols

A

inhibits breakdown of microtubules

AE: PERIHPERAL NEUROPATHY, hypersensitivity

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45
Q

How can drugs for bladder CA given through intravesicular instillation become systemic?

A

trans-urethral resection of the bladder cancer can damage bladder integrity and containment of drugs

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46
Q

-phosphomides

A

MOA: alkylating agent: inter/intrastrand DNA crosslinks
prodrug: needs activation
AE: HEMORRHAGIC CYSTITIS
give MESNA

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47
Q

MESNA

A

use with CYCLOPHOSPHAMIDE and IFOSFOMIDE to protect against hemorrhagic cystitis

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48
Q

bicalutamide

A

androgen receptor blocker (some AGONIST activity): prostate greater than central
inhibitor: CYP3A4/2C9/19,2D6

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49
Q

enzalutamide

A

androgen receptor blocker: prostate and central

AE: MALE (and female) teratogen, CNS (seizure), URTI

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50
Q

flutamide

A

androgen receptor blocker: Prostate ONLY
AE: blood dyscrasia
BBW: HEPATOTOXICITY
Tx: hirsuitism, PCOS

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51
Q

nilutamide

A

androgen receptor blocker: prostate and central
NOT teratogenic
AE: HF/HTN, blood dyscrasia, increased time for light accommodation
BBW: LUNG

52
Q

androgen receptor blocker

A

Tx: prostate CA
AE: TERATOGEN, HEPATOTOXICITY, GI, hot flash, aches

53
Q

estramustine

A

Oral
targeted alkylator attached to estradiol (binds EMBP on prostate CA): inhibits microtubules, promotes dis-assembly and G2/M arrest: produces DNA strand breaks
Testosterone levels depressed due to neg. feedback on HP axis
Tx: prostate CA
AE: GI, gynecomastia, mastalgia, impotence; EDEMA, THROMBOEMBOLISM (increased CV risk due to elevated estradiol levels), elevated HEPATIC enzymes, hyperbilirubinemia

54
Q

histrelin

A

SC
GnRH agonist
Tx: prostate CA
AE: seizure, suicide ideation

55
Q

leuprolide

A

IM/SC
GnRH agonist
Tx: prostate CA
AE: MI/HF

56
Q

triptorelin

A

IM
GnRH agonist
Tx: prostate CA

57
Q

degarelix

A

SC
GnRH antagonist
Tx: prostate CA
AE: QT PROLONGATION, HEPATIC enzyme change; HTN, impotence, weight gain, hot sweats, injection site rxn

58
Q

abiraterone

A

17-alpha reductase inhibitor (CYP17): reduce androgens by blocking pregnenolone to DHEA; progesterone to androstenedione
AE: hyper-mineralocorticoid: hypokalemia, HTN, edema (caution with pre-existing CV issues)
reduce AE: corticosteroid to suppress ACTH drive
Tx: prostate CA
other AE: HEPATIC, TERATOGEN
monitor: LFTs

59
Q

sipuleucel-T

A

immunotherapy: stimulate T cells against PAP (prostatic acid phosphatase)
culture patient APCs with PAP: APCs take up antigens and product (T, B, NK cells) re-infused into patient
Tx: prostate CA
AE: infusion rxn (fever, chill, dyspnea, N/V), paresthesia, CITRATE TOXICITY

60
Q

3B-hydroxysteroid dehydrogenase

A

converts dehydroepiandrostenedione to DHT

can lead to DHT mediated tumor activation

61
Q

use of estrogen in prostate CA
Hx?
future?

A

Hx: systemic: bone protective, CV risk

future: transdermal: no CV effects
neg. feedback decreases GnRH and therefore T; ER-beta may be protective in prostate CA

62
Q

carbataxel

A

taxol
poor P-gp substrate: decreased efflux
crosses BBB

63
Q

conventional chemo for metastatic prostate CA

A

carbataxel, docetaxel: give corticosteroids with anti-histamines to preempt edema and injection rxns (contain surfactant)
palliative for severe pain: mitoxantrone plus prednisone

64
Q

bleomycin

A

MOA: binds DNA in presence of iron with ferrous oxide to mediate DNA strand breaks
AE: PULMONARY, SKIN (rash, itch)
pulm fibrosis: injure lung epithelial cells and detected by Nalp3 inflammasome in macrophages: production of inflammatory mediators and ROS: IL-B to TGF-B

65
Q

ifosfomide

A

-phosphomide
Tx: testicular CA
AE: MYELOSUPPRESSION, HEMORRHAGIC CYSTITIS, SEIZURES (neuro)

66
Q

etoposide

A

MOA: stabilize DNA/ topo II complex: strand breaks
AE: LEUKOPENIA, hepatic, stomatitis, diarrhea

67
Q

vinblastine

A

MOA: binds B-tubulin preventing microtubule formation
AE: PERIPHERAL NEUROPATHY

68
Q

chemo for testicular CA

  1. primary
  2. second line or metastatic
  3. high dose
A

ALL: platinum agent

  1. cisplatin plus: etoposide with/out bleomycin or ifosfomide
  2. cisplatin plus: ifosfamide and microtubule drug (vinblastine or paclitaxel)
  3. paclitaxel/ifosfamide (can skip first step) followed by carboplatin/etoposide followed by peripheral stem cell infusion
69
Q

CDDP resistance

A

decrease in cisplatin sensitivity by CA cells
CA cells can: lose binding to CDDP, repair damage done by it, impair transmission of signals for apoptosis, stimulate pro-survival signals that antagonize CDDP

70
Q

amifostine

A

use with CISPLATIN to protect renal cells

71
Q

What AE do most cytotoxic (conventional) chemo drugs produce?

A

blood dyscrasia

also: GI, alopecia

72
Q

alpha 1 blockers

A

relaxation of sm. muscle in prostatic and penile urethra
metabolism: CYP
Tx: BPH
AE: xerostomia, nausea, CNS (dizzy, somnolence, insomnia, asthenia), floppy iris syndrome (adverse event can occur if have cataract Sx)

73
Q

PDE-5 inhibitors

A

inhibits breakdown of cGMP by PDE-5
CYP metabolism
Tx: ED
AE: indigestion, flushing, resp. tract infection, headache, CV, LOSS of HEARING/SIGHT
CI: NITRATES, alpha blockers (hypotension), CYP drugs

74
Q

5-alpha reductase inhibitors

A

inhibits enzyme that converts T to DHT
Tx: BPH, male pattern baldness
AE: do NOT get around pregnant women; gynecomastia, ejaculation/erectile dysfunction, decreased libido
decreases PSA (can interfere with prostate CA monitoring)

75
Q

prazosin

A

short acting alpha 1 blocker

too short and too much variability from patient to patient for use in BPH

76
Q

alfuzosin

A

alpha 1 blocker
NO CNS AE or ejaculatory dysfunction (not alpha-1a selective)
Tx: ED (off label)

77
Q

terazosin

A

alpha 1 blocker

78
Q

doxazosin

A

alpha 1 blocker

79
Q

tamsulosin

A

partially selective alpha-1a blocker

80
Q

silodosin

A

partially selective alpha-1a blocker

81
Q

tadalafil

A

PDE-5 inhibitor
long T1/2
Tx: BPH and ED

82
Q

finasteride

A

type 2 5 alpha reductase inhibitor: predominantly in urogenital tissue and genital skin

83
Q

dutasteride

A

type 1 and 2: 5 alpha reductase inhibitor: urogenital tissue and genital skin AND skin, liver, bone
long binding time: slow reversal
metabolism: CYP3A4

84
Q

beta sitosterol

A

SUPPLEMENT

Tx: BPH but does NOT reduce size of prostate

85
Q

saw palmetto

A

SUPPLEMENT

not shown to be better than a placebo in BPH Tx

86
Q

alpha-1a blockers

A

receptor predominates in prostate

Tx: BPH

87
Q

alpha-1a receptor

  1. location?
  2. advantages?
  3. disadvantages?
A
  1. lower GU tract: including prostate, prostatic and penile urethra
  2. advantages: no need for dose titration (diminished effects on CV function)
  3. disadvantages: abnormal ejaculation (none, retrograde), block CNS transmitters
88
Q

alpha-1d receptor

A

detrusor muscle of urinary bladder

89
Q

pathway of vasodilation for cGMP

A

NOS produces NO which stimulates GC which increases levels of cGMP which activates PKG leading to efflux of Ca and smooth muscle relaxation

90
Q

alprostadil

A

INTRAURETHRAL suppository, DIRECT INJECTIOn into CORPUS CAVERNOSUM: minimal systemization, rapid onset
PGE1: activates AC to increase cAMP to PKA: efflux of Ca from cell: sm. muscle relaxation
Tx: ED
AE: pain (penile, urethral, testicular), rare CV

91
Q

avanafil

A

PDE-5 inhibitor

Tx: ED

92
Q

sildenafil

A

PDE-5 inhibitor

Tx: ED

93
Q

vardenafil

A

PDE-5 inhibitor
Tx: ED
AE: QT PROLONGATION with many drugs

94
Q

methyltestosterone

A

improve response to PDE-5 inhibitors

Tx: ED

95
Q

testosterone

A

improve response to PDE-5 inhibitors

Tx: ED

96
Q

yohimbine

A

SUPPLEMENT (unregulated and often pharmaceutical strength rather than natural)
alpha 2 receptor inhibitor: blocke post synaptic adrenergic receptors and pre synaptic NANC (non-adrenergic, non-cholinergic) nerves: increases NO and sm. muscle relaxation
Tx: ED, promote weight loss, curb appetite
placebo effect causes part of the response
crosses BBB: anxiety, antidiuretic, dizzy, flush, HTN, irritable, restless, sinus tachy, tremor
MAOI action: TYRAMINE and CAFFEINE interactions
worsens: RENAL failure

97
Q

anticholinergics

A

oral
Tx: overactive bladder
CYP interactions (hepatic metabolism)
AE: DRY MOUTH and eyes, mydriasis, tachycardia (monitor for prolonged QT), constipation, urinary retention, CNS (sedation, memory, slow cognition, confusion, sleep problems)
CI: close angle glaucoma, urinary/gastric obstruction, need for mental alertness, dementia

98
Q

darifenacin

A

anticholinergic
long lasting
more selective for M3 (not clinically significant)

99
Q

fesoterodine

A

anticholinergic

100
Q

oxybutynin

A

anticholinergic: COMMON use

short lasting: have ER form

101
Q

solifenacin

A

anticholinergic

long lasting

102
Q

tolterodine

A

anticholinergic: COMMON use

short lasting: have ER form

103
Q

trospium

A

anticholinergic
long acting
quaternary amine: does not cross BBB: fewer CNS effects
NO hepatic metabolism: NO CYP interactions

104
Q

botulinum toxin

A

MOA: inhibits vesicle release of excitatory NT, inhibits axonal expression of SNARE complex dependent proteins in (sub)urothelium mediating intrinsic or spinal reflexes thought to cause detrusor overactivity; inhibition of expression of purinergic and SP receptors on suburothelial myofibroblasts
injection into urothelial wall
lasts months
Tx: overactive bladder in patients that are unresponsive to anticholinergics or patients that respond to anticholinergics but can’t tolerate side effects (works better in the latter set of patients)

105
Q

sympathomimetics

A

Tx: overactive bladder
AE: HTN, tachycardia

106
Q

mirabegron

A

sympathomimetic
B3 agonist
CYP metabolism
LONG half life

107
Q

pseudophedrine

A

sympathomimetic (off label)
direct and indirect alpha/beta agonist: alpha greater than B
AE: tachyarrhythmia, A-fib, insominia, anxiety

108
Q

ephedra, Ma Huang

A

sympathomimetic (off label)
indirect non-selective alpha and beta agonist
AE: tachyarrhythmia, CHF/MI, insomnia, CNS stimulation

109
Q

methionine

A

creates ammonia free urine by acidifying urine pH
Tx: controls ODOR, dermatitis, ulceration in overactive bladder
take with FOOD/MILK/LIQUIDS
AE: drowsy, N/V

110
Q

bovine collagen implant

A

injection into submucosa of urethra or bladder neck: increase fibers around urethral lumen
Tx: overactive bladder for those with INTRINSIC SPHINCTER DYSFUNCTION
for patients failing other therapies for more than a year
AE: urinary retention, hematuria, injection site rxn, worsening incontinence, erythema, abscess, urticaria
interactions with: immunosuppression, corticosteroids

111
Q

bethanechol

A

MOA: muscarinic agonist
Tx: urinary retention
AE: secretions (diarrhea, tears, urinate), lightheaded/syncope, dizzy, miosis

112
Q

neostigmine

A

MOA: AChE inhibitor
Tx: urinary retention
AE: hypotension/syncope, cardiac arrest/dysrhythmia, AV block, brady-arrhythmia, tachycardia

113
Q

methylnaltrexone

A

Tx: opiate induced urine retention

114
Q

naloxone

A

Tx: opiate induced urine retention

115
Q

receptors on detrusor and their actions

A
  1. SNS (hypogastric n.) release NE: adrenergic: B3; relax detrusor
  2. PNS (pelvic n.) release Ach : muscarinic: M3; contract detrusor
  3. PNS nerves release ATP: contracts detrusor
116
Q

receptors on sphincter and their actions

A
  1. SNS (hypogastric n.): release NE adrenergic: alpha 1; contract sphincter
  2. somatic (pudendal n.) release Ach: nicotinic (NOT muscarinic); contract sphincter
  3. PNS nerves release NO: relaxes urethral smooth muscle
117
Q

What can you use to treat retention?

A

cholinergic agonist

opiate antagonist

118
Q

What can you use to treat stress/urge incontinence?

A

anticholinergic

sympathomimetics

119
Q

neural circuits controlling urine storage

A

low level vesicle afferent firing

  1. spinal reflex pathway
  2. pontine storage center in rostral pons
120
Q

pontine micturition center

A

intense bladder afferent firing: possibly passes through the periaqueductal grey to reach pontine micturition center

  1. spinobulbospinal reflex pathway
  2. pontine mincturition center
121
Q

urge incontinence

A

detrusor overactivity
Sx: urgency, frequency
Tx: anticholinergics: oxybutynin, tolterodine

122
Q

stress incontinence

A

outlet incompetence
Sx: minimal urine loss with coughing, sneezing, running, laughing
Tx: topical estrogen, alpha-agonist

123
Q

mixed incontinence

A

Sx of urge and/or stress and/or overflow incontinence

Tx: focus on predominant Sx

124
Q

atonic bladder incontinence

A

Sx: complete loss of bladder control
Tx: catheterization

125
Q

functional incontinence

A

Sx: vary accourding to external cause (ex: can’t get to restroom, change in mental status, UTI, meds)
Tx: eliminate cause

126
Q

opiates

A

mu and delta receptors inhibit PNS outflow and therefore detrusor activation
AE: urinary retention
Tx: opiate antagonist (also reverses analgesia), cholinergic agonist

Reproductive (12 decks)

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