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Endocrine-Reproductive Medicine > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

What does the RAAS do?

A

BP(renal perfusion) drops, which increases renin levels, renin cleaves aniotensinogen to Angiotensin I which is converted by ACE to angiotensin II, AGII increases aldosterone, causes vasoconstriction and increases BP

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2
Q

What occurs with a 21-hydroxylase deficiency

A

cholesterol prodcuts are shunted away from mineralcorticoids and corticosteroids into the androgen pathway, this leads to low BP, hypoglycemia, weakness and virilization

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3
Q

What is 17-hydroxyprogesterone used to test for?

A

CAH or 21-hydroxylase defiency

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4
Q

What is the treatment for CAH?

A

hydrocortisone, fluids/glucose and decrease the potassium

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5
Q

What endocrine diseases are screened for in Missouri?

A

CAH and primary congenital hypothyroidism

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6
Q

What are the main causes of primary adrenal insufficiency?

A

Autoimmune adrenal destruction, TB is the most common infection, BAH due to Waterhouse-Friderichsen syndrome

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7
Q

What does increased ACTH cause on presentation?

A

increased pigmentation

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8
Q

What AR adrenal disease is familial?

A

familial glucocorticoid deficiency leading to decreased responsiveness to ACTH and it then increases

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9
Q

What are the possible deficiencies in CAH?

A

21-hydroxylase, 17-a-hydroxylase, 11-b-hydroxylase

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10
Q

How do patients present with primary adrenal insufficiency?

A

fatigue, weakness, anorexia, weight loss, hyperpigmentation(due to increased MSH), may have abdominal pain, N/V, MSK pain, psychiatric Sx, HA, sal craving, low BP, female infants will have virilization

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11
Q

What are the lab findings in primary adrenal insufficiency?

A

low Na, high K, hypoglycemia, hypercalcemia(decreased renal function), low morning cortisol with high ACTH

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12
Q

What test can confirm primary adrenal insufficiency?

A

cosyntropin test(sythnthetic ACTH), cortisol levels should increase after test

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13
Q

What lab findings are present with autoimmune Addison disease?

A

Ab to 21-hydroxylase

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14
Q

What lab finding is present in secondary adrenal insufficiency?

A

Low ACTH with low cortisol

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15
Q

What causes Cushing syndrome and what are the Sx?

A

excessive corticosteroids, central obesity, moon facies, buffalo hump, abdominal striae

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16
Q

What causes Cushing syndrome?

A

ACTH increase from the pituitary(adenoma)

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17
Q

What are 2 causes for ACTH-independent Cushing syndrome?

A

exogenous corticosteroids, adrenocortical tumor

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18
Q

What is McCune-Albright syndrome?

A

polyostotic fibrous dysplasia, cafe-au-lait spots, endocrine hyperfunction from multiple organs, causes bilateral adrenal hyperplasia

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19
Q

What is an easy screening test for Cushing syndrome?

A

dexamethasone suppression test

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20
Q

How is the dexamethasone suppression test interpreted?

A

low ACTH, not suppressed, primary hypercortisolism
elevated ACTH, not suppressed, ectopic ACTH
normal ACTH, suppressed by high dose, cushing disease

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21
Q

What are signs of primary hyperaldosteronism?

A

high aldosterone not suppressed with sodium loading

patients are hypertensive, and refractory to treatment

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22
Q

What is Conn syndrome?

A

primary hyperaldosteronism secodnary to unilateral adrenal adenoma, 40% ahve K channel gene mutation

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23
Q

What are signs and symptoms of primary aldosteronism?

A

HTN, hypokalemia, metabolic alkolosism lose protons with K

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24
Q

What is found in Von Hippel-Lindau disease type 2?

A

pheochromocytomas in 20%, AD disease, hyperthyroidism, adnexal tumors, renal cysts, adenomas, carcinomas, hemangiomas

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25
Q

What are lab findings in pheochromocytoma?

A

plasma fractionated metanepherines, single most sensitive test

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26
Q

What is the treatment for pheochromocytoma?

A

alpha-blockers, phenoxybenzamine, use prior to beta-blocker to ensure lack of unopposed alpha stimulation

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27
Q

Which MEN syndromes are associated with pheochromocytomas?

A

MEN2a and MEN2b, autosomal dominant

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28
Q

What is the linear growth rate bwtween 6yo and puberty?

A

> 5cm per year (2 inches)

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29
Q

What should you think about if children stop gaining weight early?

A

nutrition, no enough food in, not enough absorption, higher than avg caloric requirements

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30
Q

What should you think if length stops increasing first?

A

endocrine, GH deficiency, hypothyroidism, Cushing syndrome

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31
Q

What should you consider if head circumference stops increasing?

A

primary failure of brain growth, sever craniosynostosis

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32
Q

How is bone age used/determined?

A

provides a rough estimate of skeletal maturation by assessing ossification pattern of epiphyseal centers, bone age that is two standard deviations below the chronological age is considered delayed

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33
Q

How does length measurement depend on age?

A

if less than 36 months measure supine for 0-36 month chart(length), if over 24 months and using 2-20yo chart measure standing(stature)

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34
Q

What determines short stature?

A

height 2 std deviations below mean height for age and sex(<3%ile)
or, height more than 2 std deviations below the mid-parental height

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35
Q

What should be determined with delayed puberty or short stature in females?

A

karyotype, but can occur in the absence of other clinical features

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36
Q

How is precocious puberty defined?

A

full activation of HPG axis before 8yo in girls and 9yo in boys

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37
Q

What clinical findings point to precocious puberty in boys and girls?

A

girls, progressive breast development,

boys, evidence of testicular or penile enlargement, or crossing major percentile lines upward on the chart for either

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38
Q

What are common causes of DKA?

A

inadequate insulin or infection(penumonia, UTI, gastroenteritis and sepsis), infarction, surgery or drugs

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39
Q

What are some presenting symptoms with DKA?

A

anorexia, polydipsia, polyuria, N/V

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40
Q

What symptoms can come after prolonged DKA?

A

Abdominal pain, AMS, coma

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41
Q

What are signs of DKA?

A

kussmaul respirations, acetone breath(fruity), dry mucous membranes, poor skin turgor, tachycardia, hypotension, fever, abdominal tenderness

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42
Q

What lab values will be seen with DKA?

A

hyperglycemia, ketosis, metabolic acidosis, high potassium, high lipids and high triglycerides, leukocytosis

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43
Q

What does a change in pH cause potassium to do in DKA?

A

decrease in pH by 0.1 causes increase in potassium by 0.6

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44
Q

How does glucose relate to sodium in DKA?

A

every 100mg/dL of glucose over 100mg/dL causes a 1.6 meq decrease in sodium

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45
Q

What does elevate amylase suggest in DKA?

A

acute pancreatitis, or can be salivary

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46
Q

How should DKA be treated?

A

ICU, vital monitoring, glucose levels, acid base status, renal function, potassium and electrolytes

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47
Q

What is the rate of fluid replacement in DKA?

A

2-3 liters normal saline over 1-3 hours, then half normal saline at 150ml/hr, when glucose is down to 250ml/dL give D5 1/2 NS at 100-200ml/hr,
overall deficit is often 3-5 liters

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48
Q

What amount of insulin should be given in DKA?

A

10-20 units IV, then 5-10U/hr continuous, increase if no response in 1-2 hours

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49
Q

What tests should be run for underlying causes of DKA?

A

cultures, EKG, CXR, drug screen, additional history as AMS improves

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50
Q

When should potassium replacement be considered?

A

if K <5.5mEq/L, when replacing monitor EKG and renal function

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51
Q

What are thegoals of DKA treatment?

A

reduce glucose to 150-250, reverse ketonemia and acidosis, correct fluid and electrolyte balance

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52
Q

When should long acting insulin be given following DKA?

A

when patient is able to eat(no AMS, no N/V and no abdominal pain), anion gap normalization and overlap by 30-60 minutes IV and SubQ insulins

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53
Q

What are precipitating factors of NKHS?

A

insulin deficiency, inadequate hydration, osmotic diuresis due to hyperglycemia as well as sepsis, MI, glucocorticoids, phyenytoin, thiazides

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54
Q

What symptoms are common in NKHS?

A

polyuria, polydipsia, AMS, usually no N/V, abd pain, or kussmaul respirations( no ketones)

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55
Q

What labs are seen in NKHS?

A

lactic acidosis causes mild anion gap increase, moderate ketonuria from starvation, corrected sodium usually high

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56
Q

What is the treatment for NKHS?

A

ICU, monitor general status, vitals, glucose as well as acid-base status, renal function, potassium and elctrolytes

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57
Q

How should fluids be replaced in NKHS?

A

2-3 liters over 1-3 hours, then reverse deficit over next 1-2 days with 1/2 NS, when glucose reaches 250 or less switch to D5 1/2NS at 100-200mL/hr

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58
Q

How much insulin is given in NKHS?

A

5-10 units bolus, 2-7 units continuous infusion then switch with feeding as with DKA

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59
Q

What are long term complications of T2D?

A

MI, neuropathy, retinopathy, nephropathy, CAD, gastropathy, lipid deposition in eyes

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60
Q

What HgA1c is desired in diabetics?

A

below 7 but lower is better

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61
Q

What is diabetic gastropathy?

A

delayed gastric emptying, irregular nutrient delivery, insulin mismatch and hyperglycemia

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62
Q

How is proteinuria screened for?

A

spot(random) urine sample, not positive at protein under 300mg, most common protein is albumin,
microalbumin/creatinine ratio(best): detects microalbuminuria(30-300mg),
24 hr collection hard due to measurement timing and serum creatinine over time

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63
Q

How does DM impair immune function?

A

glucose over 150 interferes with neutrophils

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64
Q

What should diabetics do for foot care?

A

inspect daily, use mirror or family/friend, dont go barefoot, moisturize, prescription shoes, podiatry

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65
Q

What exams should be done yearly and quarterly for diabetics?

A

yearly- eye exam, urine protein screening, monofilament test,
quarterly- HgbA1c, SGM, foot inspection

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66
Q

How does PTH affect Ca2+ and PO4?

A

calcium increases with increase in PTH and PO4 decreases, opposite with decrease

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67
Q

How can you tell if Vitamin D is out of regulation based on labs?

A

Calcium and PO4 move in the same direction

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68
Q

What are the rapid symptoms seen with hyperparathyroidism?

A

polyuria, dehydration and renal impairment

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69
Q

What are the symptoms of chronic hyperparathyroidism?

A

kidney stones, psychiatric issues, bone problems and abdominal pain

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70
Q

When should a bisphosphonate be given?

A

patient with chronic hypercalcemia

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71
Q

What diuretic should be used in a hypercalcemic patient with HTN?

A

Loop diuretics, lose calcium

thiazides retain calcium however

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72
Q

What risks are associated with loop diuretics in hypercalcemic patients?

A

kidney stones due to increased urinary Ca and fluid shifts causing volume depletion

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73
Q

What is the difference in 1,23-OH vitamin D and 25-OH vitamin D?

A

25-OH is the storage form, 1,25-OH is active

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74
Q

Who commonly gets low Vitamin D levels?

A

elderly shut ins

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75
Q

What are the percentages of bound and unbound calcium?

A

50% is ionized(unbound), 10% bound to anions, 40% bound to protein(80% of this is albumin)

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76
Q

How is measured Ca calculated?

A

measured + 0.8(4.0-albumin)

77
Q

What levels or severity correlate with which low Ca levels?

A

mild hypocalcemia (8-8.4)
moderate <8.0 >7.5
severe <7.5

78
Q

How does immobilization affect Ca levels?

A

increased osteoclast activity, increased Ca levels in serum, PTH is suppressed, calcicuria begins, kidneys maintain homeostasis

79
Q

What is a DEXA scan?

A

dual energy XR absoptiometry, central for spin and hip and peripheral for wrist, heel, hands

80
Q

How can calcium be replaced?

A

1000-3000mg of Ca/day
Calcium carbonate is recommended but can cause constipation and upset stomach so it doesn’t get taken regularly, while calcium citrate can be taken if on H2 blockers or PPI

81
Q

What are symptoms of hyperthyroidism?

A

lid lag, exophthalmos, bruits over enlarged thyroid, HR and rhythym increase, tremor, warm moist skin, gynecomastia, muscle weakness

82
Q

What is needed to diangose Graves disease?

A

history and physical, helpful labs include supressed PTH, elevated TSI, and homogenous increased uptake of iodine by thyroid

83
Q

What medications should be considered for hyperthyroidism?

A

beta-blocker, if asthma is present calcium channel blockers can be given, anti-thyroid drugs methimazole and PTU take 2-8 wks to work, methimazole is not used during pregnancy

84
Q

When should you get a thyroid scan vs. FNA?

A

FNA if TSH is normal may be cold nodule, if low TSH go to scan to dtermine if nodule is hot

85
Q

What increases likelihood of a benign nodule?

A

FHx of benign, tenderness, mobility, Hashimoto’s, hypo or hyperthyroidism

86
Q

What increases likelihood of malignant tumor?

A

very old or young, men, Hx of neck irradiation, firm immobile nodules, lymphadenopathy

87
Q

What are symptoms of hypothyroidism?

A

sleepiness, lethargy, depression, memory impairment, inability to concentrate, goiter can be found, dry skin brittle hair, loss of eyebrows, bradycardia, decreased systolic BP, increased or decrease in diastolic BP, non-pitting edema(myxedema), decrease in perspiration

88
Q

What are the two types of epithelium on the cervix?

A

columnar and stratified nonkeratinzing squamous

89
Q

How does the SCJ change throughout life?

A

deeper inside the cervical os as child then it moves out with reproductive age and children and then back in as atrophy occurs after menopause

90
Q

How many types of HPV are considered high risk and what can they casue?

A

15 can cause cervical cancer and

CIN

91
Q

What are the 4 most important high risk HPV types and what types cause genital warts?

A

16, 18, 31, 45

6 and 11, low grade lesions

92
Q

What are risk factors for cervical neoplasia?

A

multiple partners, smoking, HIV, young age at first intercourse, organ transplant, STIs, DES exposure, high parity, infrequent pap, low socioeconomic status,

93
Q

What are the screening guidlines and ages of PAP smears?

A 
under 21: no screening
21-29: cytology q 3 yrs
30-65: HPV and cytology q 5 yrs
65+ no screening if negative previously
after hysty: no screening
94
Q

What is the Bethesda system?

A

pathologist report which indicates if specimen was adequate and any findings of dysplasia or malignancy and grading, as well as organisms,

95
Q

What type of squamous cell abnormalities can be identified on a pathology report?

A

atypical squamous-undetermined or cannot rule out high grade

LSIL, HSIL, and SCC

96
Q

What type of glandular cell abnormalities can be identified on pathology report?

A

atypical: endocervical, endometrial or glandular
adenocarcinoma: endocervical, endometrial, extrauterine, NOS

97
Q

How is ASC-US managed?

A

HPV testing preferred or retest after 1 year, if positive or still ASC then colposcopy, if nothing then return as normal

98
Q

How is LSIL managed?

A

if LSIL with neg HPV then repeat in 1 year, if LSIL without HPV test or positive HPV then colposcopy, then manage based on CIN grade

99
Q

How is HSIL managed?

A

loop electrosurgical excision or colposcopy

100
Q

What is gold standard for Dx and treatment planning?

A

colposcopy

101
Q

How is colposcopy performed?

A

wash with 3% acetic acid, dhehydrates cells and turns large nuclei white

102
Q

What should be looked for with colposcopy?

A

entire SCJ, acetowhite changes, punctations, mosaicism, abnormal vessels, then do directed biopsies or endocervical curettage

103
Q

Can the HPV vaccine be given after positive on PAP smear?

A

yes because of the other high risk strains

104
Q

What are treatment options of cerival neoplasia?

A

ablative(destroy cervical tissue) with cryotherapy or laser ablation
excisional with cold knife cone or LEEP

105
Q

When are excisonal techniques used?

A 
endocervical curettage positive(cold knife cone)
unsatisfactory colposcopy(no SCJ)
substantial discrepancy between pap and biopsy
106
Q

What are risks with excisional techniques?

A

increased risk of cervical incompetence and resultant second trimester pregnancy loss
increased risk of preterm premature rupture of membranes(PPROM)
cervical stenosis
bleeding, infection

107
Q

What are symptoms of cervical carcinoma?

A

watery vaginal bleeding, postcoital bleeding, intermittent spotting

108
Q

What are come characteristics of cervical carcinoma?

A

91% due to HPV, median age of 47, precursor lesion ten years prior, spreads by direct invasion and lymphatics, staged clincally

109
Q

How is cervical carcinoma managed?

A

microinvasion: cold knife cone or hysty
invasive early: radical hysty with lymph node dissection
bulky disease: radical hysty with lymph node dissection and cisplatin chemo
stage IIB or greater: external beam radiation and concurrent cisplatin

110
Q

What is brachytherapy?

A

radiation device is inserted into cervix and left for treatment time

111
Q

How can cervical cancer be prevented?

A

sexual abstinence/fewer partners, barrier protection, regualr exams and pap smears, HPV vaccine

112
Q

What does the HPV vaccine entail?

A

three injections second dose 2 months after 1st and then final dose is 6 months after 2nd, Age range is not 9-45 in men and women, can be given after positive HPV screen, not in pregnant patients but okay if breastfeeding

113
Q

What types of HPV vaccine are available?

A

Gardasil: quadravalent and ninevalent

Cervarix: no longer availabe but was 16 and 18 protection and only in girls

114
Q

What are side affects of HPV vaccines?

A

syncope, dizziness, nausea, HA, fever, injection site reaction

115
Q

What are the 2 general contraceptive mechanisms?

A

inhibit formation and release of egg; impose mechanical, chemical or temporal barrier between sperm and egg

116
Q

What are the two methods of comparison of birth control?

A

method failure rate(when taken correctly) vs typical failure rate(rate based of of patient usage)

117
Q

What are the forms of hormonal contraceptive?

A

oral pills, IUD, implantable rod, injectable, patches and intravaginal rings

118
Q

What does a combination OCP do to normal physiology?

A

supresses GnRH and also LH/FSH from pituitary; progesterone is the key component suppressing LH and ovulation and thickening mucous to prevent sperm migration and creating atrophic environment; estrogen stabilizes the cycle to prevent bleeding

119
Q

What are the lengths of OCP prescribing?

A

phasic- mono and triphasic; 21 days of hormones and 7 placebo or 24 and 4; continuous vs. every 3 months cycling

120
Q

What is the mini pill and what are its characteristics?

A

progestin only; makes cervical mucous thick and impermeable, ovulation continues in 40% of people; mainly in those that are breastfeeding or cannot have estrogen; must be taken at the same time everyday due to low dose and if missed by 3 hours should use back up method for next 48 hours

121
Q

What are the beneficial effects of OCP?

A

cycle regularity, improve dysmenorrhea(painful periods). decrease risk of iron deficiency anemia(short/less heavy cycles), reduced endometrial and ovarian cancer as well as benign breast disease and ovarian disease(cysts)

122
Q

What are the main side effects of OCP?

A 
serious side effects include: venous thromboses, PE, cholestasis/GB disease, stroke and MI, hepatic tumors;
breakthrough bleeding(first 3 months), amenorrhea(increases with continued use), as well as mild effects: bloating, weight gain, breast tenderness, N, fatigue, HA
123
Q

What are the characteristics of transdermal patches?

A

combination; one patch per week for 3 weeks, clean, dry skin, butt, abdomen or arm, caution in women over 198lbs, same effects as OCP but greater risk of thrombosis

124
Q

What are characteristics of the vaginal ring?

A

combination, greater compliance due to once a month use-leave in for 3 weeks, can be removed for up to 3 hours without loss of efficacy; better tolerated without GI pass and less breakthrough bleeding

125
Q

Who cannot use combination contraceptives?

A

women over 35 who smoke, history of thomboembolic events(evaluate those the FHx), women with CAD, CVD, CHF, migraine with aura, uncontrolled HTN, moderate to sever liver disease, caution in those with DM, chronic HTN and SLE

126
Q

What are charactersitics of depot medoxyprogesterone acetate injections?

A

depo provera; every 11-13 weeks IM injection; maintains contraception for 14 weeks; give within first 5 days of menses and if not use back up protection ofr 2 weeks, MOA: thicken cervical mucous, decidualization of endometrium, blocks LH surge and ovulation, efficacy similar to sterilization without weight considerations

127
Q

How does the depo shot affect bones?

A

alterations in bone metabolism with low estrogen levels, concern in adolescents, reversible after discontinuation, black box warning that if used for more than 2 years should consider alternative method

128
Q

What are side effects of depo shots?

A

weight gain; depression; irregular bleeding(25% stop in 1 year), decreasesw ith use and amennorheic after 5 years, estrogen use can improve bleeding profile, menses can take a year to regulate after stopping,

129
Q

What are indications fro depo use?

A

SZ, effective contraception, breastfeeding, compliance, contraindication to estrogen, sickle cell anemia, anemia from menorrhagia, endometriosis, decreases risk of endometrial hyperplasia

130
Q

What are contraindications of depo?

A

known or suspected pregnancy, unevaluated vaginal bleeding, breast malignancy, active thrombophlebitis or Hx of thrombembolic events

131
Q

What are characteristics of implantable Nexplanon?

A

contains etonogestrel, used for 3 yrs, insert during first 5 days of menses if not use protection for 7 days; MOA: thickens cervical mucous, inhibits ovulation

132
Q

What are side effects of implantable contraception?

A

irregular bleeding, HA, vaginitis, weight gain, acne, breast pain

133
Q

What are indications for Nexplanon?

A

convenient effective contraception; breastfeeding patients

134
Q

What are contraindications of the implant?

A

known/suspected pregnancy, thromboembolic disorder, liver tumors or disease, undiagnosed abnormal uterine bleeding, breast cancer(only absolute)

135
Q

What are the complications with insertion of the implant?

A

infection, bruising, deep insertion, migration, persistent pain or parasthesia at site

136
Q

What are the risks of IUDs?

A

infection within first 20 days, increased risk of ectopic pregnancy if it occurs, removal should be offered with pregnancy if strings are visible, reduces spontaneous abortion by 30%, risk of uterine perforation on insertion, malposition requiring hysteroscopy for removal

137
Q

What are contraindications for IUDs?

A

breast CA, recent puerperal sepsis(infection after childbirth), recent septic abortion, active cervical infection, wilson disease(copper T only), uterine malformations

138
Q

Which IUDs contain levonorgestrel?

A

mirena/kyleena for 5 years, liletta for 3 years and skyla for 3 years for nulliparous women; all highly effective 0.2% pregnancy rate

139
Q

What are the benefits of levonorgestrel?

A

decrease in menstrual blood loss, less dysmenorrhea, protection of endometrial lining from unopposed estrogen, convenient and long term

140
Q

What are charactersitics of Copper T IUDs?

A

used for 10 years, MOA: copper interferes with sperm trasnport or fertilization and implantation, same contraindications a levonorgestrel IUDs

141
Q

What are characteristics of barrier methods?

A

depend on proper use before or at time of intercourse, higher failure rate, inexpensive, little or no medical consultation

142
Q

What is the only barrier contraceptive with STI protection?

A

condoms

143
Q

What are characteristics of condoms?

A

half purchased by women, inexpensive, latex, non-latex and animal guts, reservoir tips may decrease breakage, female condoms are a thing but need to be left in for 6-8 hours after intercourse

144
Q

What are diaphragms contraceptives?

A

small latex covered, dome shaped device; used with spermicide, inserted 6 hours before and left in 6-8 after, must be fitted by healthcare individual, fit can change after childbirth, increase likelihood of of UTIs, one size fits all is Caya brand

145
Q

What is the cervical cap?

A

smaller diaphragm, applied to cervix itself, high risk of displacement and TSS, used with spermicide, left in place 6 hours after intercourse

146
Q

What is the sponge contraceptive method?

A

small. pillow shaped sponge with spermicide, fits over cervix and has elastic loop for removal, one size, more effective in nulliparous women, left in for 6 hours after but no more than 30 hrs due to TSS

147
Q

What are family planning methods?

A

calender, avoid sex during fertile period based on calendar(cycle beads); basal body temp method: check temp daily before getting out of bed, increase of temp 0.5-1 degree, do not have sex for 3 days after; cervical mucous method: when mucous changes around ovulation(spinnbarkeit), avoid sex for 4 days after; combine mucous and temp for symptothermal method as well as breast changes, cervical firmness, cramping

148
Q

What are characteristics of emergency contraception?

A

used for women who have unprotected sex, could prevent 1.5m unintended pregnancies, prevents ovulation and fertilization, no contraindications

149
Q

What are the methods of emergency contraception?

A

combined OCP method(Yuzpe) series of tablets over 72 hours; Plan B: progestin only pills 2 twelve hours apart, OTC if over 17yo, within 120 hours of intercourse, 1.1% failure rate; ella: ulipristal acetate, up to 5 days after intercourse, postpones follicular rupture/inhibit ovulation

150
Q

What is a permanent contraceptive?

A

sterilization; 1 in 3 marriages has some form

151
Q

Why do patients want sterilization and how should they be counseled?

A

permanent, know about all other options, risk/benefits, screen for regret(if young mostly), can lead to failed or ectopic pregnancy if it does occur), need condoms for STI still

152
Q

What is male sterilization?

A

vasectomy; vas deferens occlusion, safer, easier to perform and reverse, post-op hematoma, pain, infection, complete azoospermia occurs after 10 weeks

153
Q

What are characteristics of female fertilization?

A

laproscopic, hysty or at time of c-section, relatively safe, low cost, easy, permenant

154
Q

What occurs during laproscopic sterilization of females?

A

small incision, low complications; occludes fallopian tubes via: electrocautery, clips, bands, salpingectomy

155
Q

What are characteristics of electrocautery sterilization?

A

least reversible, high risk of ectopic, fast, thermal injury to other tissue

156
Q

What are characteristics of clip sterilization?

A

hulka-most reversible, greatest failure rate

filshie-lower failure rate due to large diamter

157
Q

What are characeristics of band sterilization?

A

intermediate reversibility and failure rate, more post-op pain, increased bleeding risk

158
Q

What are characteristics of salpingectomy?

A

increasing due to decreased ovarian cancer risk

159
Q

What occurs with a cystocele?

A

bladder prolapses into the vagina from the anterior(anterior vaginal prolapse)

160
Q

What occurs with a rectocele?

A

posterior vaginal prolapse; rectum pushes into the vagina

161
Q

What is an apical vaginal prolapse/uterine prolapse?

A

uterus falls down into the vagina

162
Q

What is a vaginal vault prolapse?

A

vault of the vagina falls down; these women have had hysty

163
Q

What is a urethrocele?

A

urethra collapses into the vaginal wall; can occur with cystocele

164
Q

What is treatment for anterior vaginal wall prolapse?

A

nothing, pelvic floor PT, pessary for support(ring or Gehrung), surgical correction-anterior colporrhaphy

165
Q

What is an anterior colphorrhaphy?

A

pubocervical fascia is sutured in the midline to the arcus tendinous fascia

166
Q

What is a pessary?

A

large space occupying mass that holds up the walls

167
Q

What are the treatments for uterine prolapse?

A

space filling(glehorn,donut, cude), pessary, hysty, colpocleisis

168
Q

How can you test for urethrocele?

A

PE, Q Tip test, urodynamics, postvoid residual(normal less than 50mL)

169
Q

How can urethrocele be treated?

A

topical estrogen, pelvic floor PT, pessary, subrurethral sling surgery

170
Q

What is suburethral sling surgery?

A

transvaginal tape or transobturator tape for vaginal approach;
andominal approach for Burch or Marshall-Marchetti procedure

171
Q

What is the best treatment for rectocele?

A

surgery

172
Q

What is the treatment for urge incontinence/overactive bladder?

A

behavior modification-decrease caffeine, limit fluids after 7p, bladder training; anitspasmodics: oxybutynin, tolterodine

173
Q

What are the two phases of the ovarian cycle?

A

follicular-begins with onset of menstruation and ends in LH surge;
luteal- begins with LH surge and ends with menses

174
Q

What is the 2 cell theory of the ovarian follicular development?

A

LH stimulates theca cellls to produce androgens: FSH stimulates granulosa cell to turn androgens into estrogen

175
Q

What causes the follicular phase to occur?

A

estradiol and prgesterone decrease whic causes FSH to increase then causing increase estradiol again and thus follicular growth

176
Q

What occurs during the luteal phase?

A

LH and FSH are supressed due to elevated estradiol and progesterone; no conception causes decrease in E and P and corpus luteal regession; FSH will then increase leading to follicular phase

177
Q

How does estradiol affect GnRH?

A

causes enhancement and thus mid cycle LH surge

178
Q

What does estrogen do during normal cycle?

A

low at menses then increase 1 week before ovulation; hitsp eak 1 day prior to LH peak and then falls off rising again during mid luteal phase, then back to baseline at menstruation

179
Q

What due progestins do during the normal cycle?

A

low during follicular phase from ovary and peripheral conversion adrenal pregnenolone; graafian follicle produces progesterone prior to ovulation; corpus luteum produces progesterone 5-7 days after ovulation and is at baseline before menses

180
Q

How is graafian follicle produced?

A

8-10 weeks of fetal development oocytes are surrounded by granulosa cells lead to primordial follicles which undergo development until graafian is produced, it then ruptures releasing egg; the ruptured follicle becomes the corpus luteum

181
Q

How is the corona radiata formed?

A

formed from innermost granulosa cells which have formed cumulus oophorus; the corona radiata is released with oocyte at ovulation

182
Q

How does LH causes ovulation?

A

follicular wall cells degenerate and stigma forms, the follicular BM bulges through the stigma and ruptures, releasing the oocyte into the peritoneal cavity

183
Q

How is the corpus luteum formed?

A

granulosa cells rupture and undergo luteinization; produces progesterone for 9-10 days and if no pregnancy occurs it become corpus albicans

184
Q

What are the two zones of the endometrium?

A

functionalis-responds to estrogen, sloughs off and contains spiral arteries;
basalis-remains unchanged and has basal arteries

185
Q

What are the 3 phases of the endometrial cycle?

A

mesntrual, proliferative(estrogenic) and secretory(progestational)

186
Q

What is the menstrual phase?

A

only visible phase, first day is day 1, sloughing of functionalis layer and its components

187
Q

What is the proliferative phase?

A

endometrial growth due to estrogenic stimulation; spiral arteries get longer with numerous mitoses

188
Q

What is the secretory phase?

A

dilated tortuous lumens, few mitoses, edematous stroma, endometrium at maximal thickness, spiral arteries constrict 1 day before menstruation

Endocrine-Reproductive Medicine (3 decks)

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