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Therapeutics 5 > Exam 2 part 2 > Flashcards

Exam 2 part 2 Flashcards

1
Q

Genetic sex

A 
chromosomal makeup (XY or XX)
The SRY gene is the genet hat shifts development away from female
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2
Q

Gonadal sex

A

Presence of ovaries or testes

  • Para-mesonephric (mullerian) duct- female, not fully connected
  • Mesonephric (wolffian) duct- male, turns into wolffian duct in presence of testosterone
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3
Q

Phenotypic sex

A

External or internal genitalia
Genital tubercle- develops into tip of penis or clitoris
Urogenital fold- seals and forms line of penis or labia
Labioscrotal fold- forms scrotum or labia

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4
Q

Psychological sex

A

Sex the person identifies with

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5
Q

sertoli cells

A

Secrete Mullerian-inhibiting substance (MIS) causing regression of the Mullerian ducts.

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6
Q

Leydig cells

A

Secrete testosterone which acts on the Wolffian ducts to make the epididymis, vas deferens, seminal vesicles, ejaculatory duct
DHT makes penis, scrotum, prostate

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7
Q

What merges the reproductive and urinary tracts in the male

A

Prostate

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8
Q

What does sperm production require

A

Temperatures several degrees below normal body temperature (function of scrotum)

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9
Q

Inguinal canal

A

Superficial inguinal ring is where the blood and nerve supply reach the testes. An inguinal hernia cuts off blood/nerve supply to the area.

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10
Q

Semen fluids

A

Epididymis- storage of sperm in an acidic environment (5% of semen)
Seminal vesicle- adds fructose-rich fluids, prostaglandins, and ascorbic acid. (60% of semen)
Prostate- adds phosphatase and protease rich fluids (20%)
Bulbourethral/Cowper gland- mucus secretions (15%)

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11
Q

During erection of the penis, what becomes rigid and pliable?

A

The corpus cavernosa becomes rigid

Spongy urethra remains pliable

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12
Q

Stimulation of erection

A

Release of NO (parasympathetic)

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13
Q

Ejaculation

A

Increased sympathetic input

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14
Q

Spermatogenesis

A

Occurs between tight junctions near the basal membranes (not on the blood side). You can develop antibodies against sperm if the tight junctions are not tight enough in the Sertoli cells

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15
Q

Testosterone secretion

A

Pulsatile- highest in morning
Peak 3 months gestation- formation of external genitalia
Peak 6 months old- male pattern thinking

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16
Q

Sertoli cells secrete

A

Inhibin which inhibits FHS at the anterior pituitary

Androgen binding protein

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17
Q

Sertoli cells have what receptors?

A

FSH

and aromatase allowing production of estrogen

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18
Q

Estradiol in men

A

epiphyseal closure, prevention of osteoporosis, feedback of GnRH secretion

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19
Q

Leydig cells secrete

A

testosterone which inhibits GnRH secretion at the hypothalamus and LH secretion at the anterior pituitary

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20
Q

Leydig cells have what receptors?

A

LH receptors

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21
Q

Pathologies of androgens in males during fetal life

A

Defect in 5alpha reductase- does not allow for DHT production, male genitalia does not fully develop
Androgen insensitivity- defect in androgen receptor, female appearance

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22
Q

Pathologies of androgens in males during postnatal life

A

Hyposecretion before puberty - eunichs, female characteristics but tall
Hyposecretion after puberty- may not change characteristics
Early excess secretion- precocious puberty, lack of growth. Tx with GnRH analogues

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23
Q

LH and FSH receptor abnormalities

A

McCune-Albright- precocious puberty in M and F
Activating mutations in LH- male-limited precocious puberty
Loss of function FSH receptor- infertility in M and F, amenorrhea in F

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24
Q

Normal testosterone levels

A

300-1,100 n/dL

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25
Q

Exogenously administered androgens

A

can normalize systemic levels of testosterone by not normal seminiferous tubules. Can normalize the secondary characteristics but not spermatogenesis

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26
Q

Exogenous testosterone will inhibit

A

LH and FSH (impaired spermatogenesis)

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27
Q

Long term use of testosterone can cause

A

irreversible CV disease (cardiomyopathy, atherosclerosis)

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28
Q

Types of bone

A

Spongy bone- renewed at a rate of 20%/year

Compact bone- renewed at a rate of 4%/year

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29
Q

Epiphyseal plate (growth plate)

A

Allows laying down of cartilage, which can become mineralized and allow the bone to grown in length. Mediated by GH/IGF-1 and thyroid hormone

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30
Q

Epiphyseal closure

A

Stimulation of estrogen receptors in cells of the epiphyseal growth plate leads to the conversion of cartilage into bone and terminates further longitudinal growth

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31
Q

Hydroxyapatite

A

Osteoid fluid within bone containing calcium and phosphate

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32
Q

Protein bone components

A

Type 1 collagen- vitamin C dependent. Measure through urinalysis
Non collagenous proteins- Vitamin K dependent

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33
Q

How much of plasma calcium in the active (ionized) form?

A

45%

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34
Q

What is the major site of homeostatic control of calcium

A

GI tract

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35
Q

What factors effect serum calcium?

A

Hypoalbuminemia leads to hypocalcemia

Hyperproteinemia leads to hypercalcemia

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36
Q

PTH regulation of calcium

A

PTH is magnesium dependent and comes from the parathyroid gland
It increases calcium, decreases phosphate, and increases vit D production

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37
Q

Vitamin D (calcitriol) regulation of calcium

A

increases serum calcium and phosphate

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38
Q

Calcitonin regulation of calcium

A

decreases serum calcium

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39
Q

estrogens regulation of calcium

A

inhibit bone resorption, increase Vit D, increase calcitonin

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40
Q

where does the rate limiting step of the metabolism of vitamin D occur?

A

Kidney

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41
Q

How do restore plasma calcium (in hypocalcemia)

A

decrease phosphate, increase calcium abs

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42
Q

Resorption of bone is stimulated by

A

PTH

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43
Q

Building of bone is stimulated by

A

calcitonin

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44
Q

Med causes of osteoporosis

A

aluminum-containing antacids, anticonvulsants, chemotherapy/immunosuppressants, glucocorticoids, GnRH, heparin, levothyroxine, lithium, methotrexate, pioglitazone, SGLT2i, SSRIs

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45
Q

FRAX tool

A

age, gender, prior osteoporotic fracture, femoral neck BMD, low BMI, oral glucocorticoids >3 months, current smoking, alcohol intake, parental h/o hip fractures, secondary causes of OP, RA

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46
Q

BMD screening methods

A

Central DXA (GOLD standard)
-measures BMD at total hip, femoral neck, lumbar spine
Peripheral DXA- not preferred.
-measures BMD at distal radius, heel, finger

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47
Q

T scores

A

compare bone density to the average bone density of an average, healthy 20-30 yo adult

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48
Q

Normal T score

A

Above -1.0 SD

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49
Q

Osteopenia T score

A

-1.0 to -2.5 SD

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50
Q

Osteoporosis T score

A

Below -2.5 SD

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51
Q

Screening recommendations for osteoporosis

A 
Women >65 yo
Postmenopausal women <65 with
-h/o low trauma fracture
-chronic glucocorticoid therapy
-Radiographic osteopenia
-Risk factors
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52
Q

Vertebral fracture assessment (VFA)

A

Most common osteoporotic fracutres
Lateral spine imaging with XR or VFA with DXA indicated for patietns with
-T score less than -1.0 SD AND
-women >70, men >80
-Historical height loss >4 cm (1.5 inches)
-Self reported prior vertebral fracture
-Glucocorticoids >5mg/day for >3 months
-Kyphosis

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53
Q

Osteoporosis diagnostic criteria

A

T score at or below -2.5 SD
Low trauma hip or spine fracture regardless of BMD
T score -1.0 to -2.5 SD WITH fragility fracture of proximal humerus, pelvis, or distal forearm OR high FRAX probability score

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54
Q

Nonpharm treatment of osteoporosis

A

increase vit D and calcium, exercise, smoking cessation, fall prevention, avoid excess alcohol

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55
Q

Calcium supplementation in adults >50

A

Recommend dietary intake of calcium 1200mg QD

Supplemental intake 500-1000mg calcium daily

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56
Q

Vitamin D intake >50

A

Supplemental vitamin D 800-1000 units daily

If insufficient/deficient- Vit D3 5,000 units QD for 8-12 weeks followed by maintenance therapy of 1-2,000 units QD

57
Q

Insufficient vitamin D

A

20-29 ng/dL

58
Q

Vitamin D deficient, serum

A

<20ng/dL

59
Q

Pharmacologic options for osteoporosis

A 
Biphosphonates
Calcitonin
Estrogen agonist/antagonist
Estrogen
PTH analogue 
RANK ligand inhibitor
Sclerostin inhibitor
60
Q

Estrogen agonist/antagonist MOA

A

induces osteoclast apoptosis, decreases RANKL-induced osteoclast differentiation, maintains osteoblast function

61
Q

Estrogen receptor agonist/antagonist agents

A

Raloxifene

Bazedoxifene

62
Q

Raloxifene uses

A

Prevention and treatment of vertebral fractures in postmenopausal women

63
Q

Raloxifene AE

A

thromboembolic events, hot flashes, leg cramps

64
Q

BBW of raloxifene

A

Increased risk of VTE, CV disease

65
Q

Bazedoxifene + conjugated estrogen uses

A

prevention of osteoporosis in postmenopausal women <75 yo

66
Q

Estrogen MOA for osteoporosis

A

induces osteoclast apoptosis, decreases RANKL induced osteoclast differentiation, maintains osteoblast function

67
Q

Estrogen AE

A

Nausea, HA, breast tenderness, heavy bleeding

68
Q

Estrogen uses

A

prevention of osteoporosis in postmenopausal women

69
Q

Estrogen contraindications

A

H/O or current VTE, active or h/o thromboembolic disease, thrombophilic disorder, active or h/o breast cancer, hepatic impairment

70
Q

Estrogen BBW

A

endometrial cancer, CV disease, dementia, risk vs benefit

71
Q

Calcitonin MOA

A

directly inhibits osteoclast mediated resorption

72
Q

Calcitonin uses

A

treatment of hypercalcemia. Limited efficacy in treating fractures

73
Q

Calcitonin AE

A

N, flushing, runny nose, hypocalcemia

74
Q

Calcitonin warnings

A

Long term use associated with increased risk of cancer

75
Q

Biphosphonates MOA

A

inhibits osteoclast function, induce osteoclast apoptosis

76
Q

Biphosphonates agents

A

Alendronate, risedronate, ibandronate, zoledronic acid

77
Q

Alendronate uses

A

prevention/tx of osteoporosis in men/women.

Vertebral, non-vertebral and hip

78
Q

Risedronate uses

A

Prevention of osteoporosis in women
Prevention and treatment in W and M
Vertebral, non-vertebral, hip

79
Q

Ibandronate uses

A

Prevention/tx of osteoporosis in women

Vertebral

80
Q

Zoledronic acid uses

A

Prevention of osteoporosis in women
Treatment in men and women
Vertebral, non-vertebral, hip

81
Q

Admin of biphosphonates

A

Stand or sit upright for 30-60 minutes after taking.
Zoledronic acid- IV only
Ibandronate- PO and IV

82
Q

AE of biphosphonates

A

Osteonecrosis of the jaw, atypical femur fractures (chronic therapy, more common in Asian women)
PO-dysphagia, esophagitis, ulcers
IV- flu-like symptoms

83
Q

Contraindications of biphosphonates

A

Hypocalcemia

PO- esophageal abnormalities, inability to sit upright for 30 min

84
Q

Parathyroid hormone 1-34 analog MOA

A

stimulates osteoblast function, increases calcium absorption, increases renal calcium and phosphate reabsorption

85
Q

Parathyroid hormone 1-34 analog agents

A

Abaloparatide, Teriparatide

86
Q

Abaloparatide uses

A

Tx or vertebral and non-vertebral fractures in postmenopausal women

87
Q

Teriparatide uses

A

Treatment of vertebral and non-vertebral fractures in men and postmenopausal women

88
Q

Parathyroid hormon 1-34 analog AE

A

hypercalcemia, orthostatic hypotension, muscle cramps, nausea, urolithiasis
Cumulative lifetime duration should not exceed 2 years

89
Q

Parathyroid hormone 1-34 analog BBW

A

Potential risk of osteosarcoma. Avoid in patients with Pagets disease, h/o irradiation, open epiphyses, and elevated skeletal ALP

90
Q

RANK ligand inhibitor MOA

A

monoclonal antibody against RANKL, inhibits osteoclast development and function

91
Q

RANK ligand inhibitor agent

A

Denosumab

92
Q

Denosumab uses

A

Tx of vertebral, non-vertebral, and hip fractures in men and postmenopausal women

93
Q

What osteoporosis agent is preferred in renal insufficiency?

A

Denosumab

94
Q

Denosumab AE

A

atypical femur fractures, dermatologic reactions, cellulitis, osteonecrosis of the jaw

95
Q

Sclerostin inhibitor MOA

A

monoclonal antibody against sclerostin

96
Q

Sclerostin inhibitor agent

A

Romosozumab

97
Q

Romosozumab uses

A

treatment of vertebral, non-vertebral, and hip fractures in very high risk post menopausal women.
Treatment limited to 12 months

98
Q

Romosozumab AE

A

arthralgia, hypocalcemia, atypical femur fractures, osteonecrosis of the jaw

99
Q

Romosozumab BBW

A

potential risk of MI, stroke, CV death

100
Q

When should you treat osteoporosis?

A

T score -1.0 to -2.5 with h/o fragility fracture

T score 3% or FRAX MOF >20%

101
Q

High risk osteoporosis (no previous fractures) treatment

A

Start with alendronate, risedronate, or zoledronic acid

102
Q

Very high risk osteoporosis (prior fractures) treatment

A

start with abaloparatide, romosozumab, teriparatide, zolendronic acid

103
Q

Therapeutic monitoring for pts on Rx therapy for osteoporosis

A

BMD testing q 1-2 years.

104
Q

Treatment goals of osteoporosis

A

Stable OR increasing BMD at spine or hip

No further fractures

105
Q

Candidates for gender-affirming therapy (adults) WPATH criteria

A

Persistent, thorough documentation of gender dysphoria
Capacity of informed consent
Reasonable control of other significant health issues

106
Q

WPATH criteria for puberty suppression

A

Adolescent demonstrates long-lasting and intense pattern of gender nonconformity of dysphoria
Gender dysphoria emerged or worsened at onset of puberty
Any co-existing conditions are stable
Informed consent is given and parents agree

107
Q

Irreversible effects of feminization

A

Chest growth

108
Q

Reversible effects of feminization

A

skin softening/decreased oiliness
Thinned/slowed terminal hair growth
Decreased muscle mass/strength

109
Q

Variable effects of feminization

A

fat redistribution, decreased spontaneous arousals, decreased libido, ED, decreased testicular volume and sperm

110
Q

Which estrogens are recommended for feminization?

A

Estradiol oral, SL, TD, IM

111
Q

Androgen blockers

A

suppress/minimizes male secondary characteristics. Irreversible
Spironolactone, finasteride, dutasteride

112
Q

Lab monitoring for feminization: BUN/SCr/K

A

Baseline, 3 mo, 6 mo, 12 mo, yearly, PRN if on spironolactone

113
Q

Lab monitoring for feminization: Estradiol level

A

3 mo, 6 mo, PRN

114
Q

Lab monitoring for feminization: total testosterone

A

3 mo, 6 mo, 12 mo, PRN

115
Q

Lab monitoring for feminization: Sex hormone binding globulin

A

3 mo, 6mo, 12mo if pt is complex

116
Q

Lab monitoring for feminization: albumin

A

3mo, 6mo, 12mo if checking SHBG

117
Q

Lab monitoring for feminization: prolactin

A

if clinically indicated

118
Q

General approach for feminizing hormones

A

increase both estrogen and antiandrogen until estrogen is in female physiologic range, then focus on androgen blockade

119
Q

Goal hormone levels for feminization

A

Serum testosterone <50

Peak estradiol 100-200 ng/dL

120
Q

Estrogenic therapy considerations

A

Tobacco use increases risk of CV events
Loss of erectile function
Low libido
Pituitary adenoma

121
Q

Why is blockade of feminizing hormones not recommended in masculinization?

A

Risk high for sexual side effects, CV disease, insulin resistance, and decreased bone mineral density

122
Q

Irreversible effects of masculinization

A

Scalp hair loss, deepened voice, facial/body hair, clitoral enlargement

123
Q

Reversible effects of masculinization

A

Skin oiliness/acne, increased muscle mass/strength, vaginal atrophy

124
Q

Variable effects of masculinization

A

Fat redistribution

125
Q

Which testosterones are recommended for masculinization?

A

testosterone cypionate and enanthate IM/SQ

Testosterone 1%, 1.62%, 2% gel, patch, cream

126
Q

Masculinizing therapy monitoring: estradiol

A

PRN

127
Q

Masculinizing therapy monitoring: total testosterone

A

3 mo, 6 mo, 12 mo, PRN

128
Q

Masculinizing therapy monitoring: sex hormone binding globulin

A

3 mo, 6mo, 12mo, PRN if pr is complex

129
Q

Masculinizing therapy monitoring: albumin

A

3mo, 6mo, 12mo, PRN if checking SHBG

130
Q

Masculinizing therapy monitoring: hematocrit and hemoglobin

A

Baseline, 3mo, 6mo, 12mo, yearly, PRN

131
Q

What is considered clinical response in masculinization?

A

amenorrhea by 6 months

132
Q

Masculinization recommended bioavailability of testosterone

A

> 72 ng/dL

133
Q

Testosterone therapy considerations

A

Erythrocytosis and polycythemia
Hair loss
Mental health
Cardiometabolic effects

134
Q

GnRH analogs

A

Used for pubertal suppression in central precocious puberty.
REVERSIBLE
Ideally initiate in early puberty, but not prior to Tanner 2-3

135
Q

ADR of GnRH analogs

A

injection site abscess and redness, withdrawal bleeding, hot flashes, emotional lability, HTN, weight gain, possible effects on growth

136
Q

GnRH analog agents

A

Histrelin- implanted yearly

Leuprolide

137
Q

Annual monitoring with GnRH analogs

A

Everyone- LH, FSH, metabolic (renal, liver, lipids, glucose, A1C)
With testes- testosterone
With ovaries- estradiol

138
Q

Gender affirming hormones in adolescents

A

Age >16, but individualized, may be ADDED TO GnRH analogs

Therapeutics 5 (6 decks)

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