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final Flashcards

1
Q

prefix: meno

A

menstrual related

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2
Q

prefix: oligo

A

few

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3
Q

prefix: A

A

witout/none or lack of

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4
Q

predix: dys

A

painful

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5
Q

prefix: metro

A

inbetween

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6
Q

suffix: rhagia

A

excess or abnormal (in relation to menstrual flow)

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7
Q

suffix: rhea

A

refers to flow

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8
Q

amenorrhea

A

the absence of menstrual flow

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9
Q

primary amenorrhea

A

either
1.never had a menstrual cycle and secondary sexual characteristics by age 14
2.no period by age 16 regardless of presence of normal growth and development

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10
Q

secondary amenorrhea

A

3-6 month cessation of menses after a period of menstruation

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11
Q

Number 1 cause of secondary amenorrhea

A

pregnancy
possible: menopause & lactation

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12
Q

other causes of amenorrhea

A

->defect in hypothalamic-pituitary-ovarian-axis
->endocrine disorders(hypothyroidism)
->type 1 diabetes
->some medications, illicit drug use, eating disorders, strenuous exercise, emotional stress, contraceptive use
->anatomic abnormalities

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13
Q

amenorrhea: what is done to receive a diagnosis

A

-history and physical, pregnancy testing, thyroid function tests(thyroxin), hormonal studies(prolactin (^with BF=decrease FSH)), FSH
-if never had period: pelvic exam to R/O abnormalities(could be structural problem), CT scan

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14
Q

amenorrhea: treatment

A

->primary - correction of underlying problem
->collaborative mgmt: depends on cause e.g. estrogen therapy to induce development of sec characteristics
-hormone therapy
-ovulation inducing meds e.g clomid, OCP
-calcium (for female athlete d/t decrease cal=decrease bone density)
-stress management

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15
Q

What is primary dysmenorrhea

A

-abnormally increased uterine activity secondary to myometrium contractions caused by prostaglandins
(no pathology)

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16
Q

definition: dysmenorrhea

A

pain during or shortly before menstruation

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17
Q

cause of pain for primary dysmenorrhea

A

-prostaglandin production & release by endometrium=excessive release increases amplitude and frequency of uterine contractions=vasospasm of uterine arterioles=ischemia=pain

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18
Q

secondary dysmenorrhea

A

when painful menstration is result of underlying pelvic or uterine disorder(some degree of pathology involved)
-type of pain depends on cause e.g. pelvic infection, fibroids, endometriosis

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19
Q

signs and symptoms of secondary dysmenorrhea

A

heavy, painful menstrual flow

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20
Q

diagnosis of secondary dysmenorrhea

A

physical exam, ultrasound, Dilatation and Curettage(D&C)

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21
Q

pain management for dysmenorrhea

A

-NSAIDs d/t prostaglandins
-heating pad; decrease ischemia
-hormonal birth control
-“rocking” themselves
-fetal position
-exercise; decrease ischemia + release endorphines
-hysterectomy as a last resort

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22
Q

management of dysmenorrhea

A

-prostaglandins synthesis inhibitors
-NSAIDs e.g. midol, ibuprofen, anaprox
-oral contraceptives
-diet/lifestyle style changes: decrease inflammatory foods
-comfort measures e.g. heat to abdomen, hot bath, effleurage, back massage, therapeutic touch
-reiki, acupuncture, acupressure
-herbal therapies

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23
Q

premenstrual syndrome (PMS)

A

many definitions- e.g. regular premenstrual physical and/or emotional symptoms that interfere with daily living at home and work, followed by a symptom free period
-cluster of physical, psychological, and behavioural symptoms
-does not occur if no ovarian function
-hysterectomy without oophorectomy->can still get PMS

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24
Q

common signs & symptoms of PMS

A

-anxiety
-irritability
-mood swings
-fatigue
-crying
-forgetfulness
-fluid retention
-weight gain
-breast tenderness
-impaired concentration
-feelings of loss of control
-panic attacks
-headaches
-appetite changes-binges

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25
Q

criteria of dx of PMS

A

-symptoms occur during luteal phase & resolve within a few days of onset of menses
-symptom free period in follicular phase
-symptoms are recuurent
-symptoms have a negative impact on some aspect of a women’s life
-other dx have been excluded

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26
Q

treatment of PMS

A

-seek to balance levels of hormones or serotonin, address lifestyle issues
-lifestyle/diet - decrease sodium, sugar, alcohol, caffeine, red meat, 3 small to moderate meals, 3 snacks per day rich in complex CHO and fibre, increase calcium, magnesium, vitamin E, reduce chocolate
-try to stop smoking
-stress reduction
-exercise, relaxation techniques, increased rest, yoga, massage
-support groups

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27
Q

definition of abnormal uterine bleeding

A

any form of uterine bleeding that is irregular in amount, duration, or timing that is not related to regular menstrual bleeding
e.g.trauma, infections, lesions, pregnancy, spotting

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28
Q

definition of dysfunctional unterine bleeding

A

when bleeding is related to changes in hormones that directly affect menstruation cycle
i.e. when normal cycle is disrupted, ovulation failure

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29
Q

most common cause of dysfunctional uterine bleeding

A

1.PCOS
2.hypothyroidism
3.HPI axis

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30
Q

alterations of cyclic (menstrual cycle) bleeding

A

variations in menstrual cycle such as changes in frequency, duration, or amount of flow or spotting between periods

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31
Q

oligomenorrhea

A

infrequent menstrual periods
->perhaps 40-45 days or longer
causes: abnormalities of hypothalamic pituitary or ovarian function
treatment: determine cause->hormonal therapy aka treat cause

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32
Q

hypomenorrhea

A

Short periods, with scanty blood loss, but periodas are at normal intervals
cause: often OCP. could be caused by structural abnormalities of endometrium, congenital abnormalities

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33
Q

metrorrhagia

A

intermenstrual bleeding - occurs atr a time other than normal menses
e.g. mittlestaining, “spotting inbetween periods”
treatment: depends on cause could be d/t OCP

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34
Q

menorrhagia (hypermenorrhea) (what is it and what causes it)

A

excessive menstrual bleeding in duration or amount
causes: hormonal distrubances, systemic diseases, neoplasm, infections, IUDs
treatment: depends on cause

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35
Q

definition of menopause

A

12 consecutive months without a period
-marks the end of menstrual cycles and ability to reproduce

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36
Q

definition of peri-menopause

A

the months/years leading up to menopause
-may have boughts of no period then gets it back d/t slow decrease in estrogen

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37
Q

physiology of menopause

A

ovarian function declines=decrease in estrogen lvl=eventually no menses
->endocrine system reorganizes itself. body readjusts to decrease estrogen. when new balance is acheived s&s diasappear

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38
Q

s&s of menopause

A

-hot flashes
-loss in bone density
-mood swings
-sleep disturbances
-night sweats
-dry skin, vaginal dryness
-decrease in skin elastisity
-decrease in muscle tone
-risk for cardiovascular disease

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39
Q

uterine cancer

A

-most common reproductive cancer

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40
Q

risk factors for uterine cancer

A

-ERT
-nulliparity
-obesity
-infertility
-tamoxifen
-diabetes
-late onset menopause
-PCOS
-HTN
-FHX of ovarian or breast disease
-55+
*pregnancy and OCP offer some protection since increased exposure to E&P=increased risk

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41
Q

s&s of uterine cancer

A

-irregular bleeding before or after menopause
-foul smelling and watery vaginal discharge
-pain
-B&B dysfunction

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42
Q

ability to cope with peri-menopause

A

-person’s perception or understanding of the event
-support group
-coping mechanism: positive or negative

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43
Q

attitudes towards menopause

A

can be individual, societial, cultural
-doesnt need to be negative
-30-70% of north american women experience hot flashes, 10% in other cultures; may be related to negative attitude towards symptoms/menopause

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44
Q

physical appearance of preterm NB

A

-very thin, translucent skin->can see vasculature
-very small
-underdeveloped lungs (lack surfactant before 32w)
-underdeveloped liver
-lack of antibodies from 3rd tri
-sensitive stomach & bowels->small feeds

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45
Q

stress incontinence

A

leaking or urinating due to weakened bladder muscles/structures, happens during activity that causes pressure on the bladder e.g. laughing, sneezing

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46
Q

urge incontinence

A

has a pressing urge and leakage may occur before reaching the washroom

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47
Q

treatment for stress incontinence

A

-pelvic floor exercises e.g. kegels
-biofeedback=client exercises pelvic floor muscles while connected to an electrical sensing device which provides feedback to assist with better control of these muscles
-devices that “block” the loss of urine e.g. device that fits in urethra like a plug
-surgery

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48
Q

surgery for stress incontinence

A

transvaginal taping (TVT)
anterior vaginal repair

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49
Q

treatments for urge incontinence

A

-medications: imipramine(suppresses involuntary bladder contractions) estrogen(hypoestrogenic and post menopausal women-estrogen improves muscle tone)
-biofeedback: (teaching bladder and pelvic muscle control thru positive feedback practices->see on a computer graph, audible tones when you are exercising pelvic floor muscles)
-bladder training
-bladder diet with no irritants (avoid citrus, tomato based products, caffeine, alcohol)

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50
Q

nursing care for urinary incontinence

A

-prevention->postnatal exercises
-encourage normal weight (obesity predisposes)
-good bladder habits (pee when you have to go)
-avoidance of infections
-consider psychosocial impact

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51
Q

fistula

A

abnormal opening between internal organs or between an organ and exterior of body

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52
Q

3 types of fistulas

A

most common: vesicovaginal (bladder to vagina)
-vesicocervical(bladder to cervix)
-rectovaginal(rectum to vagina)

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53
Q

cause of fistula

A

-should NOT happen secondary to childbirth (developing countries does)
-may happen secondary to congenital anomaly, gynecologic surgery, cancer, radiation therapy, or infection (episiotomy)

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54
Q

pelvic organ prolapse

A

-displacement from normal position
-usually a bulging, sagging, or falling
-various types: cystocele, rectocele, uterine prolapse

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55
Q

causes of pelvic organ prolapse:

A

-aging process
-loss of muscle tone
-genetic factors
-menopause and estrogen loss
-multiple vaginal deliveries
-severe obesity
-pelvic trauma or previous surgery
-pelvic tumour
-chronic constipation
-repetitive heavy lifting

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56
Q

signs and symptoms of pelvic organ prolapse

A

-may have stress incontinence
-vaginal/low abdominal pressure
-difficulty emptying bladder
-woman may feel like “something is in her vagina”

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57
Q

treatment for pelvic organ prolapse:

A

-vaginal pessary(ring) to support bladder and urethra
-kegel exercises
-may need surgery - anterior or posterior vaginal colporrhaphy->shortens pelvic muscles to provide better support for the bladder

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58
Q

cystocele

A

bladder “falls” & protrudes through vagina
-retained urine=risk for infection

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59
Q

rectocele

A

bowel falls & protrudes vagina
-trapped stool; risks for constipation, retained stool can get hard

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60
Q

various degrees of uterine prolapse

A

1st: slight
2nd: moderate
3rd:complete (marked)

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61
Q

signs and symptoms of uterine prolapse

A

-pelvic heaviness, pulling/dragging sensations
-pressure, lower abdominal discomfort (can feel it “falling out”)
-fatigue
-protrusions
-low backache
-dyspareunia

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62
Q

treatment for uterine prolapse

A

-pessary ring to support uterus(risk for infection, risk for necrosis if care isnt maintained)
-estrogen to increase tone

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63
Q

subtotal hysterectomy

A

removes only uterus

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64
Q

total hysterectomy

A

removes uterus and cervix

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65
Q

total hysterectomy with bilateral salpingo-oophorectomy

A

uterus+cervix+fallpoian tube(s)+ovarie(s)

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66
Q

wertheim’s hysterectomy

A

uterus+cervix+fallopian tubes+ovaries+pelvic lymph nodes+parametrium
-not common

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67
Q

signs and symptoms of ovarian cysts

A

-may be aysmptomatic or minimal pain
-menstrual irregularities
-tender, palpable mass
-if ruptured; acute pain and tenderness (may mimic appendicitis or ectopic pregnancy!)
-may cause intraperitoneal hemorrhage

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68
Q

treatment of ovarian cysts

A

if 5cm or less: oral contraceptives
if 10cm or less: laprocopy, laparotomy

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69
Q

ovarian cyst

A

follicle in ovary fills up wiht blood/fluid & creates a cyst
-able to shrink/go away on their own, some require surgery

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70
Q

dermoid cyst

A

-benigin
-can be seen in children or in ovary
-cyst develops bone & teeth & hair

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71
Q

signs and symptoms of polycystic ovarian syndrome

A

-irregular menses or ammenorrhea
-often accompanied by impaired glucose tolerance and hyperinsulinemia
-at risk for type II diabetes
-hirsutism
-obesity and acne

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72
Q

treatment for PCOS

A

1st line: oral contraceptives, weight loss, exercise, lifestyle modifications
-gonadatrophin releasing hormone for hirsutism, meds for type II to lower insulin levels

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73
Q

increased androgens from PCOS cuases

A

“male” characteristics, facial hair, acne

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74
Q

fibroids (leiomyomas)

A

benign tumours of the uterine myometrium
-very rarely become malignant
-appear to be influenced by estrogen
(estimated that 20-25% of women over 30 get them)
-increase in size with pregnancy and when taking hormones
-usually shrinks after menopause

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75
Q

signs and symptoms of fibroids(leiomyomas)

A

-may be asymptomatic
-palpable mass if tumour is large
-abnormal uterine bleeding (most common symptom)
-pain due to pressure on other organs: dysmenorrhea is a common complaint
-fatigue
-anemia if excessive bleeding
-constipation

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76
Q

treatment for fibroids (leiomyomas)

A

-myomectomy (can cause scarring=impact future pregnancies)
-gonadotropin releasing hormone antagonist (shrinks tumour)
-uterine artery embolization(enter via femoral artery & cause ischemia to the fibroid to “kill” it, but ischemia causes pain)

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77
Q

fibroids and pregnancy

A

if large they can impact the pregnancy (SGA)
-very vascular=if caught during pregnancy its avoided d/t preexisting risk for bleeding

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78
Q

what percent and age most commonly experience fibroids

A

20-25% aged 30+

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79
Q

what is endometriosis

A

a benign uterine condition in which endometrial tissue attaches to sites outside the uterus
-major cause of infertility

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80
Q

sites/implants of endometriosis

A

ovaries, fallopian tubes, peritoneum
rare; intestine, stomach

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81
Q

what causes endometriosis

A

cause; unknown
thought to be due to rertograde menstration, immune, hormonal problem, tissues travels from uterus to lymphatic or blood system, environmental

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82
Q

pathophysiology of enodmetriosis

A

-endometrial tissue responds to hormones the same way as uterine ednometrium would
-during proliferative and secretory pahses, the endometrium grows. during or immediately after menstration, the tissue bleeds, implants grow, bleed and break down
*bleeding and swelling->scar tissue around organs->pain
chronic problem

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83
Q

How hormone is endometriosis dependent on

A

estrogen dependent

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84
Q

goals of management for endometriosis

A

-relieve or reduce pain
-shrink or slow endometrial growth
-preserve and restore fertility(can cause scar tissue)
-prevent or delay recurrence(40% of recurrence if taken care of)

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85
Q

methods of management for endometriosis

A

-s&s
-history and physical
-laparoscopy
-tissue biopsy (gold standard)
-collaborative management - no cure but treatments (depends on age or woman/life plan)
-depends on extent, location, age, desire for pregnancy, severity of symptoms

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86
Q

medications for endometriosis

A

drug therapy - NSAIDs
-hormonal therapy to interrupt or stop ovulation and menstrual cycle e.g. oral contraceptives, progesterone drugs
danazol-androgenic synthetic steroid - suppresses ovarian activity - side effects
gonadotropin - releasing hormone agonists e.g. synarel, lupron (FSH & LH stimulation decrease, causes “artificial menopause”, can lead to loss in bone density)

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87
Q

Surgical management of endometriosis

A

-possible surgery
-drug therapy and surgery
-laparoscopy
-laser ablation
-may need major surgery e.g. total hysterectomy, bilateral oophorectomy and salpingectomy
-counseling, education, and support are essential

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88
Q

what medication is given to stop (or slow) premature labour? (also treats ecclampsia!)

A

magnesium sulfate (MgS4)

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88
Q

what medication is given to stop (or slow) premature labour? (also treats ecclampsia!)

A

magnesium sulfate (MgS4)

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89
Q

how many babies in canada are preterm every year? (% of births)

A

25k-30k (8% or live births)

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90
Q

what is the leading cause of infant death in NL(and canada) & how many babies are affected

A

being preterm
1 in 8 infants in NL

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91
Q

what are some serious complications for preterm infants (1/3rd of PT NB’s suffer from)

A

infections
brain bleeds
breathing problems
eye disease
life-threatening intestional disease(necrotizing enterocolitis)

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92
Q

how to assess physical maturity of a preterm nb

A

ballard assessment to estimate gestational age
-physical immaturity=physiological immaturity which can lead to short and long term complications

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93
Q

possible respiratory complications of preterm NB

A

respiratory distress syndrome (RDS)
apnea
(biggest complication)

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94
Q

possible GI complications for preterm NB

A

feeding intolerance
necrotizing enterocolitis (NEC)

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95
Q

possible complications for glucose regulation in preterm NB

A

hypoglycemia

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96
Q

possible CNS complications for preterm NB

A

intraventricular hemorrhage
thermoregulation
(bleeding into the ventricles of the brain)

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97
Q

possible vision complications of preterm NB

A

retinopathy of prematurity (ROP)
-cessation of normal eye development and subsequent abnormal vessel growth
-EXCLUSIVE to premature infants
-severity decreases with increasing gestational age

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98
Q

rationale for RDS in preterm infants

A

surfactant isnt fully developed until 34 weeks gestation=alveoli stick together

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99
Q

s&s of RDS in preterm infant

A

-INCREASED wbc
-INCREASED o2 requirements
-tachypnea
-indrawing/retractions
-grunting sounds
-may become acidotic

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100
Q

rationale for apnea & bradycardia in preterm NB

A

immature CNS=lacks signals to lungs & heart
-usually happen simultaneously

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101
Q

signs of apnea and bradycardia in preterm nb

A

-pause in breathing for 20s or longer
-sometimes w/bradycardia (<80bpm) and cyanosis
*occurs in infants less than 34wks (less prominent with increased gestational age)

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102
Q

treatment for apnea and bradycardia in preterm nb

A

-stimulation first(usually resolves it), then positive pressure(PPV) if no response(central apena)
-can be obstructive (chin-to-chest positioning), put in “sniffing position”(head elevated and tilted back so airways are open)
*trachea is all cartilage sp it occulde easily, posiitoning is v important

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103
Q

rationale for infection in preterm NB

A

no immunity acquired until 3rd trimester=0 immune system

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104
Q

s&s of infection in preterm nb

A

-temp instability(immature cns, *sepsis might decrease temp in preterm NB instead of increase (or cause variable temps)
-incraesed o2 requirements
-feeding intolerance
-vague & subtle signs (no tone/little tone, freq. A&B)
-hypotonia

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105
Q

goals of care for infection in preterm NB

A

-***prevent infection - aseptic technique & handwashin, clean environment
-early recognition of subtle signs (ref, s&s)
-early treatment

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106
Q

rationale for feeding intol. and NEC in preterm NB

A

bowels & intestines immature + imflammed with toxic gas

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107
Q

s&s of NEC in preterm nb

A

-feeding intolerance
-abdominal distension
-apnea
-lethargy
-hypotonia
-temp instability
-bloody stools
*can turn septic very quick

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108
Q

nursing care for NEC in preterm NB

A

-early recognition of subtle signs, small changes can be a sign of major complications
-early intervention and tx is critical

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109
Q

rationale for hypoglycemia in preterm NB

A

-limited glycogen + fat stores (brown fat) when PT (may start burning brown fat for glucose=uh oh)
-inability to generate glycogen d/t immature liver
-have higher metabolic demands
-thin skin=mroe susceptible to cold stress

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110
Q

s&s of hypoglycemia in preterm nb

A

-may not exhibit s&s!!
-close serum glucose monitoring as very susceptible to decerase glucose

-tx:give NB drops of colostrum or donor milk to keep BS in normal

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111
Q

rationale of intraventricular hemorrhage in preterm nb

A

immature CNS and vasculature
-most prevalent in preterm infants

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112
Q

care for intraventricular hemorrhage in preterm nB

A

-follow neuroprotective protocol if <29wks= decreased stimulation for first 72h after birth, posiiton midline + head elevated 30’, touch/talk from parent is allowed but very gentle, IV for B.G
-may have long term complications depending on severity

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113
Q

rationale for retinopathy of prematurity in preterm NB

A

prolonged exposure to high levels of o2 has a significant correlation with ROP

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114
Q

treatment for ROP in premature infants

A

-screening for ALL infants if born less than 31wks OR less than or = to 1250g weight
-if infant on o2, SPO2 should be no higher than 94-95%, if they reach this sat->begin weaning off o2 delivered, RA is considered best oractive but can receive o2 if needed (not 100%)

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115
Q

nursing care with premature infants

A

-exceptional assessment skills (small changes=big concequences)
-primary care nursing if available
-brain bundle protocol if less than 29weeks
-low stimuli environment (NICU is quiet)
-cluster care (do a lot at once then leave them alone unless needing stimulation)
-skin to skin & kangaroo care with parents after first 72h or if stable
-finger tip touch

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116
Q

common medications for premature infants

A

-iron supplement
-caffiene for apnea
-IV antibiotics if s&s of infection/sepsis

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117
Q

survival rate of premature infants

A

80% after 28weeks gestation
55% at 23 weeks
28% at 22weeks

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118
Q

rate of premature infants developing severe disabilities

A

21%

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119
Q

psychological aspect of having premature infants

A

-considered a “crisis” for parents
-fear of babies health/future
-may not be psychologically prepared for inafnts arrival
-potential separtaion in NICU

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120
Q

how to reduce negative psychological damage for parents/preterm nb

A

-encourage frequent visits
-orientate to environment
-active involvement
-phone calls, photos etc
-retain “mementos” for parents hats, measuring tape, foot prints, updates etc

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121
Q

definition miscarriage

A

loss BEFORE 20weeks gestation OR weighs less than 500g

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122
Q

define stillbirth

A

loss LATER than 20weeks OR weighs more than 500g

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123
Q

define neonatal death

A

-the death of a baby in the first 28 days of life

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124
Q

infant death: men & women grief and coping

A

-both men and women grieve with the same intensity
-women tend to seek support from tohers
-men tend to use avoid startegies such as humour or working

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125
Q

assesing timeline of infant loss grief

A

grief can last 1-2 years but never fully recovers
-within 6 months individual should have resumed some aspects of typical life

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126
Q

four pillars to caring for families (infant loss)

A

-physical care of mom
-emotional care of family
-emotional care of HCP’s(take 5 debriefing tool for staff)
-logistics (paper work, lab specimen’s etc)

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127
Q

how to support greiving families (infant loss)

A

-listen more than talk
-allow silence
-refer to baby by name (if named)
-be genuine and caring
-encourage them to see and hold baby but explain to expect baby will look like
-collect mementos and keepsakes

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128
Q

when is pregnancy and infant loss awareness day

A

october 15th

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129
Q

s&s of drug withdrawl in NB

A

jittery, irritable, shrill high pitched cry, feeding problems, yawning, increased tendon and moro reflexes(d/t CNS), diarrhea, vomiting, tachypnea, sweating, excoriation of skin, sleepiness, seizures, nasal stuffiness, increased sucking but poor appetite

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130
Q

what is critical to minimize s&s of drug use for fetus/newborn

A

education & early intervention

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131
Q

what is included in “drug use” for mothers?

A

prescription, illegal, recreational (legal), OTC, herbal, vitamins

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132
Q

most commonly abused substances during pregnancy

A

alcohol,tabacco, marijuana, cocaine, opiates

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133
Q

effects of substance abuse in pregnancy

A

-can have life long adverse consequences for baby
-outcomes vary depending on substance and level of abuse and other factors
-often born premature & SGA
-withdrawl (neonatal abstinence syndrome - NAS)

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134
Q

what can substance use during pregnancy cause

A

miscarriage, preterm labour, abrutio placentae, congential malformations

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135
Q

effects of cannabis on baby

A

-low birth weight
-preterm labour
-long-term health problems (cardiovascular & mental health)
-short & long term learning, development, & beahvioural issues
-low IQ, impulsivity, hyperactivity in childhood, may persisit to adulthood

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136
Q

women’s thoughts on cannabis during pregnancy

A

70% of women belive that there is NO risk or LOW risk of using cannabis once or twice a week during pregnancy

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137
Q

what is the most common recreational drug used during pregnancy

A

cannabis

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138
Q

how does THC get to the fetus

A

THC crosses the placenta.
THC is also store in breast milk

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139
Q

drug screening questions to be asked at every prenatal visit

A

-have you ever used drugs or alcohol during this Pregnancy
-have you had a problem with drugs or alcohol in the Past
-does your Partner have a Problem with drugs or alcohol
-do you consider one of your Parents to be an addict ot alcoholic?

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140
Q

possible signs of prenatal substance use

A

-dilated or constricted pupils
-inflamed nasal mucosa
-needl track markes, abcesses
-poor nutrition
-slurred speech
-alcohol on breath
-freq. missed appointments
-mood swings, memory lapses
-signs of agitation
-freq. accidents or falls

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141
Q

treatment for NB in withdrawl

A

-decrease environmental stimuli
-neonatal absinence scoring: finnegan scoring(determines degree of wothdrawl, dose of morphine needed, “sliding scale” morphine)
-IV morphine, decreasing dose every time possibly methadone in some centres, tincture of opium, phenobarbital, diazepam, paregonic(infrequently)

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142
Q

reasons drug addiction may occur during pregnancy

A

-role of family history
-the children of people with addictions are 8X more likely to develop an addiction
-genes for addiction
-rewiring brain
-one addicition can lead to other addictions (cross addiction)

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143
Q

long term effects of drug exposure for NB

A

-developmental delay
-learning difficulties
-concentration, attention, memory problems
-poor social judgement

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144
Q

nursing care for mother r/t substance abuse

A

-assessment during pregnancy for drug use
-may not seek prenatal care (fear of baby being taken)
-identifies babies at risk for withdrawl
-encourage parents to hold and care for baby
-educate parents on baby care and treatment
-may feel like a failure/criminal

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145
Q

nursing care of drug exposed infant

A

-fluid & electrolytes;strict intake/output
-balance small frequent feeds with rest periods->try different nipples etc possible gavage feed
-monitor weight
-reduce environmental stimuli, dim lights, decrease noise etc
-swaddle in flexed position, rock
-support self comfrting measures e.g. pacifier
-promote skin integrity
-make referrals if necessary

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146
Q

treatment for drug exposed mother

A

-interprofessional approach
-medications prescribed for opiate use by mother during pregnancy e.g. methadone

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147
Q

what may occur if NB drug withdrawl is not treated

A

D &V, dehydration, apnea, convulsions, death

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148
Q

families in recovery (FIR) combined care unit

A

-rooms mom & drug exposed baby together
-promotes comforting and healing for both mom and baby
-reduces symptoms of withdrawl in baby and decreases need for drugs to sooth withdrawl symptoms

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149
Q

define large for gestational age (LGA) macrosomia

A

typically above 90th percentile on the intrauterine growth chart for gestational age

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150
Q

risk factors for macrosomia (large for gestational age)

A

-excessive weight gain in preg
-fetal exposure to high estrogen levels
-high maternal birth weight
-LGA in previous infants
-maternal diabetes
-maternal pre pregnancy obesity
-multiparity

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151
Q

associated complications for macrosomia (large for gestational age)

A

birth trauma, hypoglycemia, congenital anomalies

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152
Q

define small for gestational age (SGA) AKA IUGR-intrauterine growth restriction

A

typically below the 10ht percentile on the intrauterine growth chart for gestational age
*may look premature but if term they will have no issue with corrdinating the suck/swallow reflex

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153
Q

maternal risk factors for SGA(IUGR)

A

anemia, diabetes, malnutrition, smoking

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154
Q

uterine/placental risk factors for SGA(IUGR)

A

placental abruption, placenta previa, infection

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155
Q

FETAL risk factors for SGA(IUGR)

A

birth defects, multiple gestation, infection

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156
Q

birth trauma

A

-can occur during vaginal or C/S birth
-can be a result of prolonged or difficult labour(dystocia), assisted birth
-assessment of NB is critical

157
Q

nursing care for birth trauma

A

swaddling, gentle handling, promotion of comfort

158
Q

birth asphyxia

A

-anything that causes lack of perfusion to the baby
-develops from inadequate o2 transfer during labour and birth

159
Q

birth asphyxia interventions

A

-1st intervention: stimulation
-may require PPV with bag and mask
-too much o2 can cause oxidant injury! use RA
-chest compressions and intubation may be required

160
Q

meconium aspiration

A

meconium in amniotic fluid increases risk of meconium aspiration
-meconium can lead to rupture of alveoli

161
Q

meconium aspirations interventions/care

A

-if infant is not vigourus at birth; temporarily intubate and suction meconium prior to stimulation with drying (if vigourus let them clear it on their own)
-complications can be minimized
-endotracheal intubation and suctioning performed
-requires close assessment and monitoring

162
Q

respiratory distress

A

-can happen at term but preterm is higher risk
-critical for NB to be oxygenated
-RDS may become apparsnt shortly after birth r/t deficiency of surfactant/lung maturity
-cannot sustain the work of breathing
-administration of antenatal steroids help mature fetal lungs (helps decrease the risk of severe lung disease & resultant hypoxia after delivery
-tracheal tugging, nasal flaring, sternum sucking in

163
Q

congenital anomalies

A

-genetic factors and teratogenic exposure are associated with congenital anomalies (dysmorphology)
-when one major congenital anomalie is present, the nurse is alert to other anomalies

164
Q

nurses role; congenital anomalies

A

-v important to teach women about congenital anomalies (ie: teratogens - embryonic heart starts beating only 24 days after conception, important to teach about avoidance of teratogens preconception
-prevention is the main goal, if not possible the nure can be involved with early detection and begin providing information and preparing parents
-“dont talk with your face”
-speak matter of factly and explain well

165
Q

drugs used for chlamydia

A

azithromycin, doxycycline

166
Q

drugs used for chlamydia during pregnancy

A

amoxicillin, erythromycin, azithromycin

167
Q

medication for genital herpes

A

valacyclovir(valtrex), famcyclovir(famvir), acyclovir(zovirax)

168
Q

medication for syphilis

A

penicillin

169
Q

medication for varicella zoster

A

acyclovir

170
Q

medication for candidiasis

A

monistat, nystatin

171
Q

medication for group B strep

A

IV broad spectrum antibiotics

172
Q

TORCH infections

A

infections that can cause serious problems for baby

173
Q

what does TORCH stand for

A

T-toxoplasmosis
O-other: chlyamydia,gonorrhea, syphillis
R-rubella
C-cytomeglavirus
H-herpes

174
Q

antepartal meaning

A

during pregnancy

175
Q

placenta previa definition

A

placenta is implanted in the wrong spot in the lower uterine segment
-over or very close to the cervix

176
Q

complete placenta previa

A

cervix completely covered by placenta
*-c-section needed bc if cervix starts to dilate & efface that causes abruption

177
Q

partial placenta previa

A

cervix is partially covered by placenta

178
Q

marginal placenta previa

A

placenta implanted very close to cervix
*-may be allowed yo delivered vaginally, still high risk of hemorrhage

179
Q

with placenta previa fundal height will be ___ higher

A

2-3cm

180
Q

low lying placenta

A

placenta implanted less than 2cm from cervix

181
Q

clinical manifestations of placenta previa

A

-painless, vaginal bleeding, bright red
-vitals may be normal(due to extra BV)
-fetus may be in abnormal position
-blood clotting is usully normal(mom’s clotting factors remain normal since it won’t detect bleeding)
-signs of fetal hypoxia(if maternal shock or extensive placental detachment)
-fetal/neonatal anemia possibly

182
Q

uterus characteristics with placenta previa

A

soft and non tender

183
Q

clinical manifestations: placenta previs with thinning and strectching of LUS

A

-disruption in placental blood vessels, increased risk of bleeding as term approaches & effacement and dilation occur, disrupts placental attachement.

184
Q

why is there an increased risk of bleeding with placenta previa?

A

-abruption occurs d/t dilation and effacement of cervix
-uterus isnt able to contract to stop blood flow
-can leave to severe bleeding episode

185
Q

complications of placenta previa

A

-PROM
-preterm L&D
-anemia
-uterine rupture
-PP infection
-PP hemorrhage
-fetal death(d/t hypoxia)

186
Q

when is a c-section necessary for placenta previa

A

1.complete placenta previa
2.2.bleeding is sufficient to jeopardize mother or baby

187
Q

management for placenta previa

A

-depends on length of gestation and amount of bleeding
-homecare possible if 1.stable 2.no active bleeding 3.can get to hospital quickly, if not=hospitalization

188
Q

if woman has placenta previa, is less than 36wks gestation and is NOT in labour & bleeding has stopped what occurs?

A

bed rest & close observation to allow time for fetus to mature
-d/t risk v benefit of lvl of bleeding vs gestational age

189
Q

nursing care for placenta previa

A

-monitor amount of bleeding on pad
-bed rest/limited activity
-vitals
-o2 if required
-monitor fetus
-assess for s&s of shock or contractions
-IV fluids
-know blood type
-no PV exam
-corticosteroids if < 34weeks

190
Q

abruptio placentae (placental abruption)

A

-premature seperation of a normally implanted placenta from the uterine wall
-accounts for significant maternal & fetal morbidity and mortality
-associated with highestrates of intrauterine death

191
Q

partial placenta abruption

A

when only a portion of the placenta detaches

192
Q

complete placental abruption

A

when the placenta completely detaches from the uterine wall

193
Q

marginal/apparant placental abruption

A

only the edges “margins” of the placenta detach and bleeding is visible

194
Q

central/concealed placental abruption

A

the centre portion of the placenta detaches, and bleeding is concealed since the edges remain intact

195
Q

clinical manifestations of placental abruption

A

-sudden, sharp, and severe onset of abdominal or back pain(d/t blood pooling)
-uterus is firm and board-like(d/t being filled with blood, may “feel contractions”)
-bleeding may or may not be visible
-may have signs of shock
-risk for DIC d/t clotting factors activated=decreased platelets in cirulation
-often decerased variability or late/variable decels on FHR

196
Q

nursing priority for placental abruption

A

-ABC’s: bleeding & establish circulation
-IV N/S or R/L to keep BV up
-transfusion of blood & platelets (prevent shock & DIC)
-management depends on maternal & fetal status
-if condition deteriorates=c-section

197
Q

fetal presentation/response to placental abruption

A

-usually normal presentation
-response depends on amount of blood loss & extent of uteroplacental insufficency

198
Q

complications of placental abruption

A

-preterm birth=SGA
-neuro damage to baby d/t hypoxia
-DIC
-pp hemorrhage
-infection

199
Q

management if preterm & experiences placental abruption

A

-try to preserve pregnancy as long as possible
-steroids to accerlate fetal lung maturity if bleeding is stabilized or mild abruption

200
Q

nursing care for placental abruption

A

-close monitoring of mother & fetus
-observe for shock, bleeding
-measure abdomen/ fundal height for accumulation of blood
-assess discomfort/contractions
-establish IV access and give iv fluids
-catheter; I&O monitoring
-o2 if fetal distress
-may need corticosteroids(for fetal lung development if preterm)

201
Q

3 ways how are placental abruption and placental previa differentiated

A

1.type of bleeding(A-bleeding may be concealed or apparent P-bright red bleeding every time)
2.-uterine tonicity(A-boardlike P-soft & nontender)
3.-presence ot absence of pain(A-painful abd or back pain, P-painless)

202
Q

3 things care of late pregnancy bleeding is based on

A

1.gestational age(term or not)
2.amount of bleeding
3.fetal condition

203
Q

placenta accreta

A

“A” for** a**ttached really well
-attaches too strongly to muscle layer of uterine wall (myometrium)

204
Q

placenta increta

A

“I” for invasive
-invades into myometrium/endothelial tissue

205
Q

placenta percreta

A

“P” for protrusion
-invades beyond uterus and attaches to adjacent orgens (bladder, bowels etc)
-hysterectomy is needed to remove it all therefore C-section is required

206
Q

how can invasive placenta be detected prior to birth

A

-ultrasound

207
Q

risk factors that cause invasive placenta

A

previous c-section=8x higher risk for accreta d/t scar tissue

208
Q

maternal risks of invasive placenta

A

-risk for maternal hemorrhage
-risk for hysterectomy(precreta)
-cause of maternal mortalitiy
-may lose parts of bowel or bladder (precreta)

209
Q

vasa previa

A

“velamentous cord insertion”
-fetal vessels running into or coming within close proximity to the internal cervical os
-risk of blood vessels rupturing

210
Q

disseminated intravascular coagulation (DIC)

A

-over activation of the clotting cascade and the fibrinolytic system resulting in depletion of the platelets and clotting factors
-ALWAYS A SECONDARY DX
-often triggered by release of large amounts of thromboplastin

211
Q

causes of DIC in pregnancy

A

damage to vascular integrity
-placental abruption
-retained demised fetus”missed abortion”
-amniotic fluid embolis
-severe preeclampsia
-sepsis

212
Q

S&S of DIC

A

-unusual spontaneous bleeding i.e. gums, eyes or nose
-petechaie (especially after blood pressure cuff inflation)
-execessive bleeding from puncture sites i.e.IV
-tachycardia & diaphoresis

213
Q

1st trimester with pre-existing diabetes

A

-maternal blood glucose lvls drop by 10% d/t E&P stimulating the beta cells in the pancreas:)
-diabetes will be better controlled, insulin requirements will drop
-blood glucose also drops d/t: N&V, decrease in appetite with 1st tri, & fetus using a lot of blood glucose

214
Q

2nd & 3rd trimester with preexisting diabetes

A

key word: insuling resistence
-placenta develops HPL(human placental lactogen) around 20wks which have anti-insulin properties
-HPL then enters maternal circulation & destroys her insulin=increased B.G=more glucose going to baby=makes insulin less effective to ensure enough glucose for bb
-creates 2-4x the need for insulin
-bigger the placenta=more HPL

215
Q

what does HPL contain

A

cortisol + insulinase

216
Q

if maternal glucose levels increase then

A

fetal glucose levels increase

217
Q

increased fetal glucose levels then

A

increases fetal insulin levels = insulin promotes fetal growth

218
Q

since maternal insulin cannot pass through the placenta… when does the fetus start producing their own insulin

A

10 weeks gestation

219
Q

what does uncontrolled maternal diabetes increase risk for in NB

A

-congenital abnormalities e.g. CHD, spinal defects
-RDS(hyperinsulinemia in fetus alters surfactant production)
-hypoglygemica, hypocalcemia, hyperbilirubinemia, hypomagnesemia, polycythemia, cardiomyopathy
-miscarriage, infection, dystocia(d/t macrosomia)

220
Q

how does gestational diabetes occur?

A

when non-diabetic people cannot compensate for the HPL process

221
Q

when is insulin supplementation needed in gestational diabetes

A

when BG is 7.8mmol/L or higher during glucose tolerence test

222
Q

when is a glucose tolerence test performed during pregnancy?

A

24-26 weeks

223
Q

what is one test performed at prenatal visits to monitor for diabetes?

A

-urine dip
-assesses for glucose & ketones in urine (can develop acidosis if ketones present)

224
Q

how is gestational diabetes managed?

A

-usually diet & exercise alone can control it
-some cases may need insulin (>7.8mmol/L)

225
Q

Glucose tolerance test to diagnose gestational diabetes

A

drink solution of 50g glucose->check BG in 1 hour
-if BG is 7.8-11.1=diabetes
-if >7.8, test is repeated with 75g glucose+fasting
-FPG=>5.3, 1hrPG=>10.6, 2hrPG=>9=diabetes
-if BG is >11.1=diabetes

226
Q

vascular remodelling

A

-normal in pregnancy
-blood vessels widen to accomodate increase in BV

227
Q

defective remodelling

A

-abnormal in pregnancy
-no or partial accomodation for increased BV

228
Q

patho of defective remodelling

A

inadequate vascular remodelling=increased PVR=increased B/P(vasospasm)=decreased placental perfusion(hypoxia)=endothelial cell dysfunction! which= increased cell permeability->act of coagulation cascade->vasoconstriction

229
Q

patho of HTN in pregnancy

A

causes decreased tissue perfusion=increased vascular premeability=leakage of intravascular proteins & fluids(EDEMA!!)=decreased plasma volume-> can lead to HELLP

230
Q

what does HELLP stand for

A

Hemolysis
Elevated Liver enzymes
Low Platelets

231
Q

patho of HELLP syndrome

A

-endothelial cell dysfunction d/t fibrin deposits + formation of fibrin mesh decreased vascular premeability
-platelets adhere to blood vessels=narrows vessels
-destruction of RBC’s bc they get push thru narrowed vessels=anemia
-decreased cirulating platelets d/t clotting=DIC risk
-increased liver enzymes=tonic clonic seizures(=no perfusion to fetus=hypoxia)=high mortality rate

232
Q

H->hemolysis in HELLP

A

red blood cells get damaged as they pass thru narrowed vessels d/t fibrin deposits

233
Q

EL->elevated liver enzymes in HELLP

A

endothelial damage and fibrin deposits cause impaired liver function resulting in elevated liver enzymes

234
Q

LP->low platelets in HELLP

A

increased platelet destruction/adhesion of platelets in blood vessels=low circulating platelets (DIC risk)

235
Q

drugs used to treat HTN in pregnancy

A

-magnesium sulfate(MgS04):blocks neuromuscular transmission and assists with vasodilation
-nifedipine: Ca channel blocker
-labetalol: beta blocker
-hydralazine: reduces vascular smooth muscle improving blood perfusion
-furosemide: diuretic, inhibits reabdorption of Na and Cl

236
Q

signs of magnesium sulfate toxicity

A

-smooth muscle relaxtation: RR<12, weakness, paralysis, dec. urinary output, absence of deep tendon reflexes

237
Q

what is antagonist for magneium sulfate

A

IV calcium gluconate

238
Q

managment/nursing care while on magnesium sulfate for preeclampsia

A

-low stimulus environment
-catheter->strict I&O(I:usually no more than 120ml/H d/t may get pulmoanry edema or cerebral edema)
-wtach for toxicity d/t dec. kidney fucntion=dec. output=build up of Mgs04

239
Q

assessment of fetal status w/preeclampsia

A

-kick counts(6 per 2h)
-NST weekly or biweekly
-may need biophysical profile(BPP) or ultrasound

240
Q

pre-existing hypertension

A

present before pregnancy or diagnosed before 20 weeks

241
Q

gestational hypertension

A

normotensive previously, develops after 20 weeks

242
Q

what is preeclampsia (mild & severe)

A

HTN after 20 weeks + proteinurea

243
Q

what is HELLP syndrome a complication of

A

preeclampsia + involvement of other systems

244
Q

what are risk factors for preeclampsia

A

-diabetes
-some paternal influence
-drugs
-family hx
-obesity
-nutrition
-extreme maternal ages (<20 or >40)

245
Q

patho of preeclampsia

A

-if defective remodelling occurs or partially occurs=decreased placental perfusion + hypoxia
-this placental ischemia is thought to cause endothelial dysfunction which then leads to 1.vasospams 2.inc. peripheral resistance 3.inc. endothelial peremability

246
Q

main pathogenic factor of preeclampsia

A

NOT an increase in BP but rather poor perfusion as a result of vasospasm & reduced plasma vol
-endothelial cell dysfucntion causes many of the S&S

247
Q

patho of kidney damage in preeclampsia

A

decreased kidney perfusion->decreased GFR & output->inc serum sodium, BUN, uric acid, and creatinine->glomerular damage->fluid shift->edema & relative hypovolemia=inc viscosity in blood
-also protein (primarily albumin) lost in urine

248
Q

protein dipstick urine values for mild & severe preeclampsia

A

mild: +1-+2
severe: +3-+4

249
Q

patho of decreased liver circulation of preeclampsia:

A

->impaired function
->hepatic edema, hemorrhage, thrombosis, hepatic necrosis
-elevated liver enzymes
-woman may complain of epigastric or RUQ pain

250
Q

patho of decreased perfusion to brain preeclampsia

A

->hemorrhage, edema, and vasospasms
->headaches, visual disturbances (blurred or double vision)
->CNS irritability (hyperactive deep tendon reflexes, seizures, positive ankle clonus)

251
Q

decreased placental function for preeclampsia can lead to

A

->increased risk of placental abruption->intrauterine growth restriction(IUGR), premature birth, early degenerative aging of the placenta

252
Q

SPASMS (preeclampsia s&s acronym)

A

s-significant BP changes may occur without warning
P-Proteinurea->serious sign of renal involvement
A-Arterioles are affected by vasospasms that result in endothelial damage and leakage of intravascular fluid into the interstitial spaces(edema)
S-Significant labratory changes (most notably Liver Function Tests (LFT) and the platelet count), signal worsening of the disease
M-Multiple organ systems can be involved: CV, hematological,hepatic,renal, and CNS
S-Ssymptoms appear after 20 weeks

253
Q

general s&s of preeclampsia

A

-very vague, epigastric pain (late), flu-like symptoms, N&V
-develops and progresses rapidly
-early signs may not be noticed

254
Q

first sign a woman may notice of preeclampsia is:

A

-weight gain (more than 1lb a week) due to fluid retention that causes edema

255
Q

women with preeclampsia are at an increased risk for :

A

adverse perinatal outcomes in a FUTURE pregnancy

256
Q

what is checked at every prenatal visit to rule out preeclampsia

A

-weight
-BP
-urine(protein)
-check for edema

257
Q

managment/nursing care for mild preeclampsia

A

-BP 140/90 or ^ x2 at least 4-6h apart OR increase of sys >30 and dys >15 (if known)
-proteinurea: +1 or +2; normal urine output
-headache usually absent but could be transient; no abd pain or visual probs etc
-no signs of kidney or liver involvement
-normal fetal growth depsite dec. placental perfusion

258
Q

management/nursing care for severe preeclampsia

A

dys: >110 sys: >160
-proteinurea +3 or +4 dipstick
-fetus below expected growth (IUGR)
-brisk tendon reflexes
-CNS S&S-continous headache, drowsiness, menal confusion
-visual disturbances
-elevated hepatic enzymes (alt, ast, LD)
-dec. urine output
-numbess in hands or feet
-epigastric painominous sign(developing HELLP)
-THROMBOCYTOPENIA

259
Q

nursing care of SEVERE preeclampsia

A

-V/S & edema checks q1h-q4h depending on severity
-auscultate breath sounds
-continuous FHR monitoring if MgS04
-check LOC
-neuro checks (H/A, visual issues, epigastric pain)
-check brachial & patellar clonus
-lab: daily liver enzymes & platelet
-IV fluids & electrolytes (no more than 125ml/Hr)
-s&s usually resolve within 48h

260
Q

what is ecclampsia

A

onset of seizure activity or coma in a woman with preeclampsia
-no hx of pre-existing patho

261
Q

what % of eclamptic women develop ecclampsia while pregnant

A

70%

262
Q

what % of women develop eclampsia in the immediate postpartum period

A

30%

263
Q

eclampsia (tonic clonic) can lead to:

A

cerebral hemorrhage, premature seperation of the placenta, severe fetal hypoxia, PROM, pulmonary edema, circulatory or renal failure

264
Q

eclampsia nursing care/managament

A

-ensure airway & client safety(seizure)
-position on side following convulsion
-oxygen, suctioning, start IV (MgS04)
-assessment of uterine activity, cervical status, & fetal status
-lab tests; liver enzymes & platelets

265
Q

what is a high risk pregnancy?

A

condition/s which threaten maternal and/or fetal health or interferes with normal fetal development, childbirth, or transition to parenthood

266
Q

psychological effects of high risk pregnancy

A

-increased stress
-uncertainty about outcomes
-disruption of family routitines, role changes, child care issues, work disruption etc
-may have difficulty establishing relationship with fetus if outcome is questionable
-hospitalization is a source of stress
-guilt is very common

267
Q

goals of nursing care for HR pregnancy

A

-reduce incidence of health issue affect mom and or baby by identifying risk factors & s&s
-treat ASAP
-minimize effects of complications on pregnancy outcome
-monitor status of pregnancy
-emotional support

268
Q

risks of adolescent pregnancy

A

-can affect education & career options
-many dont seek antenatal and follow-up care
-often poor nutritonal status
-smoking & substance abuse common
-insufficient weight gain, ED’s
-^ Fe deficiency anemia
-^LBW, ^preterm birth
-^risk of abuse to child
-^GHTN
-cephalopelvic disproportion(CPD)

269
Q

nursing care during adolescent pregnancy

A

-assess mom’s/partners/families/friends reaction=highly influenced
-assist girl in experincing physically safe and emotionally satisfying pregnancy, promote optimal health for mother and baby
-educate re: options
-provide support, treat with respect, no judgement
-assess devlopmental lvl
-encourage prenatal care & education

270
Q

multiple pregnancy (twins) high risk

A

-goal: reach 36-37 weeks with all fetuses developing normally
-close monitoring (doppler studies, BPP, NST)
-consider high risk d/t cord entanglement, fetal comprimise, & placental abruption
-method of birth depends on positon of 1st fetus

271
Q

cardiovascular disorders during pregnancy

A

-normal changes during pregnancy impact woman with pre-existing cardiac disease
-normal heart can compensate for ^ BV
-diseased heart cannot compensate well - if not well tolerated, can lead to cardiac failure during pregnancy, L&D, or PP period
-consider degree of disability rather than type of diagnosis when considering TX and prognosis

272
Q

autoimmune disorders (lupus) in pregnancy

A

-disrupt the formation of the immune system
-occur frequently during reproductive years
-can affect the course of pregnancy or are harmful to fetus
-close monitoring before, during, after pregnancy
-body can produce antibodies against fetus

273
Q

cholelithasis

A

-gallstones in gallbladder
TX: diet change during preg (risky to do surgery)
-hypothesis during pregnancy: estrogen causes increased cholesterol secretion of bile; progesterone promotes decreased gallbladder motility
-hormones+pressure from uterus=messes with normal circulation & drainage of the gallbaldder
-most are ASYMPTOMATIC; may have epigastric (RUQ) pain that radiated to back & shoulders
-may be spontaneous or after high fat meal

274
Q

cholecystitis

A

-inflammation of gallbladder
-causes: gallstones obstructs a cystic duct; pressure from uterus interfere with normal circulation and drainage of the gallbladder
-high risk: older pregnant women w/ several pregnancies & history of previous attacks
-more severe epigastric pain than cholelithiasis
-N&V, fever may be present
-could be hospitalized to rule out preeclampsia

275
Q

treatment for gallladder conditions

A

-antibiotics, analgesics, IV fluids, bowel rest, & NG suctioning
-surgery should be postponed until postpartum period
-recurring may require immediate cholecystectomy - preferably during second trimester, but can be performed anytime during pregnancy

276
Q

Effect of antepartal hemorrhagic disorders

A

-increases in plasma volume & RBC’s: 1.meet metabolic demands of mother & fetus
2.protect against potentially poor venous return
3.protect the mother against blood loss at birth
-maternal blood loss=dec. o2 carrying capacity to tissues/organs/fetus(ischemia/fetal hypoxia)
-any bleeding in pregnancy inc. risk of maternal &/or fetal morbidity & mortality

277
Q

common causes of bleeding in trimester 1

A

-mostly spontaneous abortion

278
Q

common causes of bleeding in tri 2-3

A

-placenta previa
-placental abruption
-abnormal implantation(invasive placenta) and/or development of placenta
-trauma

279
Q

medical term for pregnancy lost before 20 weeks

A

abortion

280
Q

4 types of abortion

A

a)spontaneous
b)voluntary
bI)elective
bII)therapeutic

281
Q

miscarriage of 3 more consequtive pregnancies

A

habitual abortion

282
Q

what % of pregnancies end in miscarriage

A

10-15%

283
Q

when was abortion decriminlaized in canada

A

1988

284
Q

management/nursing care for abortion

A

-confirm pregnancy & gestation; bimanual exam/US
-blood work
-pre-abortion counselling
-mostly D&C and vaccum aspiration
-nursing support during procedure
-recover for 4-5h them go home
-rhoGAM to woman who is Rh neg

285
Q

client teaching/primary concepts of abortion

A

-expect some cramping, bleeding like heavy period
-often prophylactic antibiotics
-NSAIDs for pain
-avoid douching, sex, tampons for approx 2 weeks
-expect next period in 4-6weeks
-contact dr if s&s of infection
-info re:birth control
-follow up w/ dr

286
Q

imcomplete spontaneous abortion (miscarriage)

A

-some products of conception are left behind
-cervix often stays opne & hemorrhage is very common
-DIC is very common

287
Q

causes of spontaneous abortion (miscarriage)

A

-geentic anomalies
-uterine or cervical problems, infections, substance abuse, maternal conditions (e.g. diabetes, hypothyroidism)

288
Q

threatened spontaneous abortion (miscarriage)

A

-fetus still viable, cervix is closed
-small amount of bleeding
-think fetus “threatened” to abort but didnt

289
Q

inevitable spontaneous abortion (miscarriage)

A

-cervix is open, lots of blood coming thru, pregnancy will definately be lost

290
Q

complete spontaneous abortion (miscarriage)

A

-inevitable turns into complete
-nothing is left in uterus

291
Q

missed spontaneous abortion (miscarriage)

A

-fetus stops developing, but fetus stays in the uterus
-abortion need to be induced

292
Q

management for threatened abortion

A

-priority=hemorrhage->infection->pain->psychological
-may require IV
-blood work(type, Rh, Hbg, Hct)
-date of LMP
-obstetric history
-vital signs
-bed rest, nutritious diet, adequate hydration

293
Q

nursing care for threatened abortion

A

-decrease stress
-no sex
-emotional support;determine meaning of pregnancy for this woman

294
Q

management/care following spontaneous abortion

A

-may require dilation and curettage (D&C)
-follow up - phone calls
-referal as necessary
-may have mood swings
-expect cramping
-monior bleeding
-assess pain
-eat high iron and protein
-support groups
-avoid pregnancy for at least 2 months to allow recovery

295
Q

6 methods of abortion

A

1.methotrexate
2.suction curettage or vacuum aspiration
3.dilation and curettage(D&C)
4.misoprostol(prostaglandins)
5.RU 486: mifepristone “abortion pill”
6.mifepristone with misoprostol

296
Q

2 types of second trimester abortions

A

-dilation & evacuation (surgical)
induction of labour with misoprostal and oxytocin(medical)

297
Q

gestational trophoblastic disease aka “molar pregnancy”

A

-a tumour develops in the uterus from conceptual tissue
-monitoring hCG lvls for 12 months
-risk of choriocarinoma(if any of the cysts are left behind)
-avoidance of preganancy for 12 months + regular follow ups(produced hCG for up to 12m, need to monitor dropping lvls)

298
Q

ectopic pregnancy

A

embryo attemots to implant in a site other than the uterus, commonly; fallopian tubes, ampulla, less commonly; abdominla cavity, cervix
-leading cause of infertility
-life threatening

299
Q

causes/risk factors for ectopic pregnancy

A

aka anything that caused blocked or narrow fallopian tubes
-previous pelvic infection
-(most common)hx of chlamydia
-previous appendicitis
-hx of infertility or c-section
-age 35 or higher
-smoking

300
Q

clinical manifestations of ectopic pregnancy

A

-positive pregnancy test
-vaginal bleeding
-abdominal pain
-bladder pain
-dizziness,pallor,nausea
-cullen’s sign(bruised blueness around umbilicus d/t blood pooling in abdomen)
-can lead to severe hemorrhage and shock
-if rupture occurs= increased pain from blood in perineum. causes referred pain in shoulder tip d/t internal bleeding irritating the diaphragm

301
Q

diagnosis of ectopic pregnancy

A

-rule out other conditions e.g. abortion
-US->transvaginal,abdominal,laparoscopy to dx
-if previous positive pregnancy test, repeat hCG levels over 48 hours

302
Q

treatment of ectopic pregnancy

A

-depens on if its ruptured or not
-drugs (unruotured) methotrexate(prevents fetal cell growth & divison)
-laparoscopic surgery
-supportive nursing care; gentle upon palpation, may fear for safety & express concern for fture fertility, psych health w/pregnancy termination (pregnancy loss NOT abortion)

303
Q

How to treating ectopic pregnancy (surgical or nonsurgical)

A

-non surgical: methotrexate (unruptured) disrupts growth of developing embryo->cessation of pregnancy
-surgical; unruptured, removal by salpingostomy(fallopian tube is maintained, developing fetus is removed)
-surgical is ruptured; laparoscopic salpingectomy(fallopian tube removal)

304
Q

influences on newborns risk of impaired thermoregulation

A

-immature thermoregulation system(hypothalamus)
-large heads (most of heat is lost there)
-thin skin & little subcut fat
-inability to shiveress than internal core temp
-air temperature l

305
Q

evaporation heat loss

A

-loss of heat when water is converted to a vapor (wet skin->heat loss)

306
Q

conduction heat loss

A

loss of heat to a cooler surface by direct skin contact e.g. cold hands

307
Q

convection heat loss

A

loss of heat from warm body surface to cooler air current e.g. cold breeze, o2 administration

308
Q

radiation heat loss

A

-losses occur when heat transfers from heated body surface to cooler surfaces and objects not in direct contact with body e.g.near a cold window

309
Q

heat loss in NB results in:

A

-peripheral vasoconstriction
-increased metabolic rate
-increased voluntary muscular activity(moving limbs in attempt to warn up (cant shiver))
-decreased BG d/t using it for warmth(appears restless)
-increased RR

310
Q

compensatory mechanisms to maintain core heat include:

A

1.nonshivering thermogenesis
2.-use of brown fat stores(doesnt regenerate and may cause metabolic acidosis or jaundice )
3.-increased respirations (tachypena)

311
Q

nonshivering thermogenesis

A

production of heat thru lipolysis of brown adipose tissue (fat) it is metabolized to produce heat

312
Q

where is brownfat found in NB’s

A

mid scapula, around neck, axillae, deeper placenment around trachea, esophagus, abdomen, aorta, kidneys, adrenals

313
Q

hyperthermia in newborns s&s

A

-temp above 37.5
-can cause increased heart, respiratory, and metabolic rates->increased o2 consumption, dehydration from h2o loss(extreme sweating) and peripheral vasodilation(flushing) which may cause hypotension

314
Q

purpose of gluconeryl transferase

A

-makes bilirubin water soluble so it can be excreted in urine & stool

315
Q

what value of bilirubin need to be reached in the first few days after birth for the NB to be VISIBLY jaundiced

A

85-120umol/L

316
Q

physiological process make jaundice so common in NB’s

A

-liver is still immature
-NB RBC’s live for 70 days (120days in adults)
-rate of bilirubin production is higher than the rate of elimination(inc. conc. in bloodstream)
-limited binding sites on albumin for bilirubin (inc. conc in circulation)

317
Q

why does jaundice make babys skin & sclera yellow?

A

uncoagulated jaundice is deposited in skin and mucous membranes
-value reaches 85-120umol/L

318
Q

teaching points about jaundice for parents

A

-imporant to know s&s since it’s neurotoxic and can cause kernicterus
-baby should NOT be sleeping through the night. need to be woken up & feed

319
Q

4 causes of jaundice

A

1.physiological jaundice(apparant in 3-5 days)
2.pathological jaundice(apparent in 24h)
3.non-physiological (breastfeeding jaundice, breast milk jaundice (late onset))
4.blood group incompatibility(Rh or ABO incompatibilities)

320
Q

what billirubin levels can cause kernicterus(neurotixicity)?

A

340umol/L

321
Q

what is breast milk jaundice?

A

-late onset
-occurs after first week once true milk is established->peaks at ~2-3wks
-related to composition of milk
-some womens milk may contain elevated conc of free fatty acids
-may compete with bilirubin for binding sites on albumin & inhibit bilirubin conjugation or increase lipase activity=increasing circulating bilirubin

322
Q

what is breastfeeding jaundice?

A

-early onset, day 2-4
-approx 10-25% of breastfed babies
-possibly due to decreased caloric & fluid intake until milk “comes in”
-feed q2-3h
-colostrum=natural laxative, leads to mec passage which decreases bili lvls (bilirubin is eliminated in urine and feces)

323
Q

blood group (ABO) incompatability

A

when mother & babies blood groups do not match and mom’s antibodies causes fetal blood cells to clump together-> they are hemolyzed and produce larger quantities of bilirubin
-effects are mild, usually treated with phototherapy

324
Q

hydrops fetalis

A

large amount of fluid build up in baby causing edema
-caused by rhesus incompatibility

325
Q

erythroblastosis fetalis

A

when fetal red blood cells are destroyed by maternal circulation due to ABO incompatibility
-prevented using RHOgam

326
Q

6 possible events leading to Rh sensitization (fetal and maternal blood with opposite Rh factors mix)

A

1.Rh neg mom becomes pregnant with 1st Rh pos baby
2.at birth Rh pos cells enter mom’s circulation
3.moms tissue produce anti Rh antibodies
4.2nd Rh pos child is conceived(antibodies from preg 1)
5.moms anti Rh antibodies pass thru placenta into fetal blood supply
6.fetus develops HDN as moms anti Rh antibodies & Rh antigens cause babys RBCs to react and clump together

327
Q

what maternal conditons will warrant use of RHOgam

A

1.ectopic pregnancy
2.aminocentisis
3.blood transfusion w/ Rh pos blood
4.miscarriage
5.abortion
6.trauma
-mom is neg for antibodies after Rh pos baby, given rhogam within 72h of birth

328
Q

what does RHOgam do

A

prevents mom from reacting to antigens of her incompatible fetal cells after birth
-causes cells death of fetal Rh pos cells before mom can develop antibodies

329
Q

indirect vs direct coombs test

A

-test for antibodies on RBCs
-direct: tests RBC’s
-indirect: tests serum in the blood

330
Q

if baby is effected by rehsus incompatability and requires transfusion what is given?

A

-neonatal exchange transfusion of type O Rh neg RBC’s
-treats anemia & helps remove bilirubin, mom’s antibodies & fetal RBC that are starting to clump
-not done often due to RHOgam:)

331
Q

when is an exchange transfusion needed in jaundice?

A

-if jaundice fails to respond to phototherapy
-requires close monitoring & V/S
-recheck bili lvls after infusion

332
Q

what is an exchange transfusion (used to treat jaundice)

A

-blood is withdrawn from umbilical vein & donor blood replaces amount
-done 2-10ml at a time
-can be done at room temp rather than warmer (4h limit)

333
Q

prenatal care for rhesus incompatibility

A

-indirect coombs test
-may need intrauterine blood transfusion (Rh neg type o via umbilical vein)
-indirect coombs test repeat at 28 weeks (if neg give rhogam)
-if pos, test repeated throughout pregnancy to determine degree of severity

334
Q

s&s of hyperbilirubinemia (jaundice)

A

-yellow discolouration of skin & sclera
-dark or tea coloured urine; decreased urine
-dark coloured or discoloured stools
-decreased feeding or excessive sleepiness during feedings
-poor suck reflex
-hypotonia/lethargy
-kernicterus

335
Q

screening for jaundice

A

TcB & TSB done at same time, at discharge or at 72h of life
-if jaundice prior to 24h, bilirubin test (pathological jaundice)
-short hospital stay=increased risk (3-5 days to develop)

336
Q

managment/ nursing care phototherapy for jaundice

A

-expose as much skin as possible(roll down diaper)
-eye pads on at all times
-reposition q2h
-check stools for colour and amount (bili excretion + acidic stools so change often & quick)
-monitor temp q2h
-increase fluids
-I&O
-3h in then remove for 3h for sensory & feeds
-no oil on skin (even vaselin on bum)
-arrange your care

337
Q

other effects of phototherapy on baby

A

-vasodilation (monitor temp)
-increased insensible water loss(increase fluids)
-skin rashes
-hyperthermia
-lethargy
-Bronze Baby syndrome
-loose green stools(excretion of photodegradation products)

338
Q

goals of nursing care during phototherapy

A
  1. ENSURE SAFETY:eye protection, feeding to reduce fluid loss & dehydration)
    2.ASSESSMENT & MONITORING: improvement of jaundice/skin colour/temp/feeidng behaviours/expulsion of excessive bili
    3.MAINTAIN PHYSICAL & DEVELOPMENTAL HEALTH: diaper care, no creams or oils, frequent stimulation q2h
339
Q

the process of normal respiratory adaptation to extrauterine life

A

1.birth canal compresses fetal chest; as chest emerges ait is sucked into lungs (reason why c-section babies are more mucousy)
2.clamping of umbilical cord affects chemo-receptors
3.fluid in alveoli is absorbed into pulmonary lymphatics; fluid replaced by air
4.surfactant supports respiration by lowering surface tension and prevents alveolar collapse
5.systemic vascular resistance increases
6.shunts close (FO &PDA)
7.blood circulates through lungs
8.baby changes from blue to pink

340
Q

3 fetal structural changes of the heart include

A

1.closure of foramen ovale
2.closure of ductus venosus
3.closure of ductus arteriosis

341
Q

the process of normal blood circulation adaptation to extrauterine life

A

1.clamping of umbilical cord closes placental circuit
2.rapid changes in pulomary vascular resistance
3.systemic vascular resistance increases=reduces right to left shunting & sends blood thru lungs
4.blood bypasses foramen ovale & it closes and seals
5.rise in o2 lvls cause ductus arteriosis to begin to constrict immediately after birth (functionally closed by 96h after birth)
6.vasodilation of pulmonary blood vessels decreases pulomary vascular resistance (increase blood flow thru lungs)
7.baby changes from blue to pink

342
Q

what may be a risk with delayed cord clamping

A

jaundice d/t increased RBC’s
intraventricular hemorrhage d/t excess blood

343
Q

when is the cord typically clamped in NL

A

60s

344
Q

immediate care of newborn

A

priority: airway
-be prepared to resus
-note time of birth
-cord clamping
-provide warmth
-infection control
-apgar scores

345
Q

apgar score of 0-3 indicates

A

severe distress

346
Q

apgar score of 4-6 indicates

A

moderate difficulty adjusting

347
Q

apgar score of 7-10 indicates

A

minimal or no difficulty adjusting to extrauterine life

348
Q

early newborn care procedures

A

-ID bands
-measurements/weight
-med admin: vit K, erythromycin eye ointment
-head to toe + reflexes(physical and neuro assessment)
-gestational age assessment(ballard scale)
-behavioural assessment(extrauterine adjustment)
-skin-to-skin(first hour)
-first bath(24h)

349
Q

3 ways gestational age can be assessed

A

1.maternal menstrual history (aka due date)
2.ultrasound exam
3.ballard scale (gestational age assessment)

350
Q

complications of post-term infants

A

-aging placenta=placental insufficency=poor oxygenation & nutrient transfer
-dry, cracked, wrinkled skin
-hypoxia, LGA, meconium aspiration syndrome, hypoglycemia, jaundice, polycythemia

351
Q

initial period of reactivity

A

-first 30 minutes
characteristics: alert, active, strong desire to suck=optimal to breastfeed
-may be tachypneic and tachycardia
-may have mild to mod chest retractions, nasal flaring, expiratory grunting, period breathing, acrocyanosis, bowel sounds active (all this can last 7-10 days)
implications: minimize bright lights to encourage them to open their eyes, good time for interaction, strengthens bonding & attachment

352
Q

period of relative inactivity

A

-after first period of reactivity, occurs 2-3h after birth
characteristics: period of decreased responsiveness, falls asleep, difficult to arouse, feeding difficult or impossible, HR stabilizes(110-160) resps decrease to 40-60, centrally pink, temp may drop
implications: good time for mom and baby to rest

353
Q

second period of reactivity

A

-begins to wake from first sleep
-occurs roughly 4h after birth & lasts 10m to several hours
-alert and responsive again, HR and RR should be in normal limits
-may pass first meconium, readiness for feeding again
-good time for family to visit

354
Q

deep sleep in newborn

A

eyes closed, no eye movement, reg breathing, not easily aroused

355
Q

light sleep in newborn

A

periods of REM, resps irregular, random movements, startles easily

356
Q

drowsiness in newborn

A

eyelids flutter, delayed response

357
Q

quiet alert in newborn

A

very interested in surroundings, bright look, attends to stimulation

358
Q

newborn screening

A

-glucose testing (if indicated)
-new metabolic screening i.e. PKU
-auditory screening
-cystic fibrosis screening
-post-discharge follow up->48h

359
Q

a parent asks about follow ups with community health nurse/doctor what do you say?

A

visits at 48h, 1 weeks, and 6 weeks, more if needed

360
Q

what is circumcision & nursing care provided

A

can occur as a sterile elective procedure or spirtual/cultural ceremonial act
-yellen clamp or plastibell procedure
care: 1.alleviate pain 2.prevention of infection

361
Q

goals of care with a healthy newborn

A

-maintain patent airway
-maintain stable temp
-protect from infection and injury
-provide optimum nutrition
-promote parent-infant attachment
-prepare for discharge and home care

362
Q

3 phases of maternal adjustment

A

taking in
taking hold
letting go

363
Q

taking in phase

A

-dependency on HCP
-woman wants to talk about her experiences

364
Q

taking hold phase

A

woman starts to focus more on NB instead of herself
- begins to initiate care on her own

365
Q

letting go phase

A

-readjustment of relationship
-adjusts to new role/lifestyle as a mom
-PPMD may start to set in

366
Q

3 things partner may experience while adjusting to new role

A

1.formation of fatherhood identity
2.competing challenges of new fatherhood role
3.changes and restrictions in lifestyle

367
Q

postpartum blues

A

-self limited
-affects 70% of women
-symptoms peak @ ~4 days PP and decrease by 10 days-2 weeks PP

368
Q

postpartum depression

A

-may last for weeks or months
-can develop anytime within the first year after childbirth
-etiology: may be hormonal imbalance and predisposition; past personal or family hx of psych disorders; poor maternal health, lingering PP blues

369
Q

primary infertility

A

man or woman who has never been able to conceive

370
Q

secondary infertility

A

inability to conceive after one or both partners have previously conceived

371
Q

reasons why infertility rates may be on the rise

A

-family hx
-environmental factors
-age
-increase in ART
-increase in availability & use of reproductive services

372
Q

% of imapired fertility explained

A

1/3 woman, 1/3 man, 1/3 combined

373
Q

causes of female infertility

A

-decreased progesterone
-ovulatory problems
-age
-infections
-tubal problems
-genetic conditions
-stress
-smoking, alc, drugs, caffeine
-probs with cervical mucus & uterine conditions
-environmental factors
-congenital abnormalities

374
Q

causes of male infertility

A

-sperm production
-abnormal morphology
-transport problems
-ED
-hypospadias
-smoking, alc, drugs
-use of medications

375
Q

infertility treatment available in NL

A

IUI (intrauterine insemination)
-picks out best sperm and injects them into uterus as close to fallopian tube as possible

376
Q

why do you have to take your temp every morning with IUI

A

-temperature increases when ovulating, uses that to guage when to do injection

377
Q

cost of IUI

A

$1000 per cycle (15-20% chance of fertilization=multiple cycles)
-NL subsidy of 5k per cycle up to 3 cycles

378
Q

tests of womans fertility

A

-assessment of the hypothalamic-pituitary axis in terms of ovulatory function
-assessment of structure and function of uterus, fallopian tubes, ovaries

379
Q

evaluation of ovulatory factors

A

-basal body temp recording
-hormonal assessments of ovulatory function: gonadotropin lvls(FSH,LH), progesterone, prolactin, thyroid hormones, estradiol
-endometrial biopsy
-abdominal or transvaginal ultrasound

380
Q

evaluation of cervical factors

A

-cervical mucus
-pre-ovulation: scant/sticky
-as estrogen increases: more copious & clear
-at ovulation: elasticity or “spinnbarkeit” increases and viscosity decreases
-following ovulation - progesterone increases->mucus is scant, sticky & thick

381
Q

what is spinnbarkeit

A

german word for stretchable
-mucus is stringy, stretchy, quality of the cervical mucus found especially around time of ovulation

382
Q

testing of man’s and couples fertility

A

-semen analysis; done prior to invasive tests on women
-post-coital test(evaluates sperm in cervical mucus)

383
Q

methods of managing infertility

A

-cryosurgery
-meds to restore cervical & vaginal pH to normal
-hormone tx; induce ovulation e.g. clomid
-surgery- laser to correct some problems
-lifestyle/diet changes
-herbal remedies

384
Q

common ART’s

A

-intrauterine insemination(IUI)
-in-vitro fertilization(IVF)
-donor oocytes or sperm
-surrogate motherhood
-gamete intrafallopian tranfer(GIFT)
-new ones developing all the time

385
Q

infertility support groups

A

-infertility awareness association of canada(IAAc)
-canadian fertility and andrology society
-newfoundland and labrador fertility services

386
Q

informational erasure & inclusive reproductive care

A

lack of knowledge of trans people & the assumption that knowledge of trans people & reproduction does not exist

387
Q

institutional erasure & inclusive reproductive care

A

lack of polices that include trans people

388
Q

transnormalitivity

A

trans people must either be “man” or “woman” to be legitimate to other people, no true for everyone

389
Q

barrier to gender inclusive care

A

-availability of services
-stigmas based insociety
-cisnormativity/heteronormativity
-transphobia
-lack of knowledge from HCP
-hormone therapy disrupting fertility & gender dysphoria

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