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z S1: Module > Endocrine-2 > Flashcards

Endocrine-2 Flashcards

no med chem of male reproductive

1
Q

Naturally occurring estrogens

A

17β-estradiol > estrone > estriol

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2
Q

Estrogen is synthesized from what two things

A

androstenedione or testosterone

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3
Q

Anterior Pituitary Gonadotropins

A
  • Luteinizing Hormone (LH)
  • Follicle Stimulating Hormone (FSH)
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4
Q

Trophoblast gonadotrophin

A

Human chorionic gonadotropin (hCG)

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5
Q

Gonadotropin Receptors

A

FSHR: FSH
LHR: LH, hCG

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6
Q

Growth/maturation _________ follicle of ovary

A

Graafian

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7
Q

Corpus Luteum hormones

A

Progesterone, Estrogen

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8
Q

Endometrium:

A

endothelial lining, stroma

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9
Q

myometrium

A

smooth muscle

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10
Q

Perimetrium

A

outer serous coat

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11
Q

Follicular phase

A

estrogen builds endometrium
* Cell proliferation, increased thickness
* Induction of progesterone receptor

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12
Q

Luteal phase

A

progesterone prepares for implantation
* Ends estrogen effects on growth
* Stimulates endothelial secretions
* Blood vessel growth

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13
Q

Post-implantation

A

Stimulates LHR in corpus luteum to maintain
estrogen, progesterone synthesis

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14
Q

What does the ERalpha and ERbeta estrogen receptors do

A

ERα: female reproductive tract, mammillary gland, hypothalamus, endothelial cells, vascular smooth muscle
ERβ: Prostate, ovaries, lung, brain, bone, vasculature

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15
Q

Osteoblasts

A

↑ synthesis, type I collagen, osteocalcin, osteopontin

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16
Q

Estrogens plasma bound: _______________________ (SHBG) albumin

A

sex-hormone binging globulin

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17
Q

Single PR gene; two main isoforms: PR-A and PR-B which is inhibitory and which is excitatory

A

PR-A - inhibitory
PR-B - excitatory

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18
Q

Ligand-binding: dimerization, binding to what

A

progesterone response element (PRE)

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19
Q

What are Anti-progestins and Progestin Modulators used for

A

Early pregnancy termination

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20
Q

Ulipristal acetate (ELLA)

A

progesterone receptor modulator/partial PR agonist
inhibits ovulation
emergency contraception

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21
Q

Anti-Estrogens: “Pure” Estrogen Antagonists

A

Clomiphene and Fulvestrant

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22
Q

Estrogen Modulators/Anti-estrogens

A

Tamoxifen, Raloxifene, Clomiphene, Fluvestrant

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23
Q

Aromatase Inhibitors: steridal and non-steridal

A

Steroidal: formestane, exemestane (AROMASIN)
* irreversible
Non-steroidal: anastrozole (ARIMIDEX), letrozole (FEMERA), vorozole
* Reversible

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24
Q

Effects of estrogen

A

-Maturation of the female reproductive organs
-Maintains skin & blood vessels / & thickness of the vaginal lining
-↓ the resorption (breakdown) of the bone by osteoclasts
-↑ the coagulability of the blood
-Normal development of the endometrial (uterine) lining
-Can increase various hormone binding globulin

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25
Q

Progesterone during pregnancy and menstrual cycle regulation

A

During pregnancy – it maintains the endometrial lining
Menstrual cycle regulation – cyclical development & shedding of the endometrial lining

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26
Q

Androgens

A

Androstenedione is a weak androgen; it is converted to testosterone in the periphery
Testosterone & dihydrotestosterone (DHT) have significant androgen activity

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27
Q

_____ has a greater affinity for the androgen receptor and is the more potent androgen

A

DHT

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28
Q

Available LARC methods

A

copper IUD
levonorgestrel IUD
etonogestrel SUBDERMAL IMPLANT

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29
Q

copper IUD MOA

A

Primary – continual release of Cu++ into the uterine cavity Copper ions toxic to sperm; ↓ viability, ↓ motility

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30
Q

levonorgestrel IUD MOA

A

Primary – LOCAL effect; continual local release of progestin into uterine cavity
-Thickens the cervical mucus (sperm traveling up to the uterus is difficult)
-Over time causes changes to and thinning of the uterine lining

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31
Q

etonogestrel subdermal implant MOA

A

Primary – controlled release of progestin; suppresses ovulation
Thickens cervical mucus & produces a thinner endometrium

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32
Q

LACR return to fertility

A

1-2 cycles

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33
Q

Estrogen component actions

A

Helps prevent ovulation (estrogen will inhibit FSH production)
Regulates proliferation of the endometrial (uterine) lining; provides cycle control
Prevents the adverse effects of estrogen deficiency on various things

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34
Q

Elimination of estrogen

A

extensive 1st pass hepatic metabolism primarily by CYP450 3A4 enzymes

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35
Q

ethinyl estradiol

A

the synthetic estrogen used in almost all CHC products Available in oral doses containing
(usually 20mcg as starting dose)

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36
Q

Progestin component actions

A

-Suppression of LH - ↓ response of the ovary to FSH; LH surge is inhibited
-Thickens cervical mucus
-Slows ovum transport through Fallopian tubes
-Continuous use produces an atrophic endometrial lining

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37
Q

____________ an analog of spironolactone; has anti-mineralocorticoid activity

A

drospirenone

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38
Q

Risk of Estrogen: venous thromboembolism

A

[deep vein thrombosis (DVT), pulmonary embolism (PE)]

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39
Q

Risk of estrogen: CV disease

A

↑ risk occurs in women > 35yrs; especially if a heavy smoker
-contraindicated in smokers over 35 yo
-contraindicated with any ASCVD event

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40
Q

Risk of estrogen: Hypertension

A

Systolic BP ≥160 or Diastolic BP ≥100 is a contraindication to CHC
Systolic BP ≥140-159 or Diastolic BP ≥90-99 – generally should not use CHC, R>B

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41
Q

Risk of estrogen: breast cancer

A

several large population-based studies have NOT found a significant association btw the use of CHCs and breast cancer; do not use with a personal history of breast cancer

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42
Q

Risk of estrogen: headaches w/ focal neurological deficits what is contraindicated

A

Use of CHC

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43
Q

Risk of estrogen: breastfeeding concerns

A

Estrogen decreases breastmilk production
CHC are approved if breast milk is well established
Do not start until > 6 weeks postpartum

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44
Q

Traditional “21/7” cycles

A

mainly monobasic (same dose of E/P)
-the progesterone ingredient has more effect on the side effects not the phases
-the standard recommendation is to start on a monobasic

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45
Q

Who benefits from a entended or continuous cycle birth control

A

severe menstrual cramps
excessive bleeding
endometrial pain
-increased breakthrough bleeding

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46
Q

What is the day 1 start

A

initial pack started on 1st day of bleeding
no backup needed

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47
Q

What is a sunday start

A

initial pack started on 1st Sunday after period started
back needed for 1st week
no period on the weekend

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48
Q

What to do if 2 or more pills are missed

A

use a non-hormone backup method until active hormone tabs have been taken for 7 days

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49
Q

Side effects of too much estrogen

A

nausea/vomiting/bloating (take at night)
HTN
headache
darkened pigmentation

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50
Q

Side effects of too little estrogen

A

amenorrgea
vaginal dryness
BTB

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51
Q

Side effects of too much progesin

A

fatigue
mood changes
headache

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52
Q

Side effects of too little progestin

A

BTB

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53
Q

Side effects of too much androgen activity

A

acne
decreased libido
increased appetite
weight gain

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54
Q

Recommendations for adverse effects of birth control

A

an adequate trail for any pill should be 3 months
most side effects disappear by 4th cycle

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55
Q

Birth control serious ACHES

A

abdominal pain
chest pain
headaches
eye problems
severe leg pain

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56
Q

Transdermal Patch for non-daily contraceptive

A

3 wk on / 1 wk off
if women is >90 kg its a decreased efficacy
increases risk of VTE

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57
Q

Vaginal ring for non-daily contraceptive

A

3 wk on / 1 wk off (use new ring)
<3 hr then efficacy not affected
no douching

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58
Q

Progestin-only contraceptives: norethindrone MOA

A

increase thickness of cervical mucus (harder for sperm to move)
no placebo days
late by 3 hrs is a missed pill

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59
Q

Why are POPs the preferred oral contraceptive pill during breast feeding

A

they do not effect milk production and no clotting risk
can start right after pregnancy

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60
Q

What is the OTC progestin only pill

A

norgestrel (Opill)

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61
Q

Depo-injection

A

suppress FSH/LH
endometrial thinning
-cause weight gain
-BTB
-decreased bone mineral density (BMD)
takes 6-12 months for fertility to return

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62
Q

Copper IUD emergency contraception

A

if placed w/in 5 days of intercourse it is the most effective method
increased BMI does not decrease effectiveness

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63
Q

Ulipristal Acetate emergency contraception

A

SPRM (block progesterone from binding to receptor)
Inhibits or delays ovulation from occuring
give w/in 5 days

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64
Q

High dose progestin-only tablet for emergency contraception

A

inhibit or delay LH surge
levonorgestrel (PlanB)
take w/in 3 days

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65
Q

Yuzpe Method of emergency contraception

A

uses combo w/ high dose of progestin
causes nausea and vomiting

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66
Q

Comparative effectiveness of EC (highest to lowest)

A

copper IUD
ulipristal acetate
OTC levonorgestrel
Yuzpe

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67
Q

Indications for using topical corticosteroids

A

relieve dermatitis
eczema
ano-genital itching
external vaginal itching

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68
Q

MOA of corticosteroids

A

anti-inflammatory decrease production of mediators
immunosuppressive
anti-proliferative

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69
Q

Potency of topical corticosteroids

A

chemical structure modification
vasoconstrictor assay
potency classification
vehicle formulation

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70
Q

As a general rule ointments and gels are more or less potent than creams and lotions

A

more

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71
Q

Enhanced absorption effects of topical corticosteroids

A

skin hydration
occlusive dressings

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72
Q

Age of patient in relation to topical corticosteroids

A

-younger and older tolerate lower potency
-infants use the mildest topical in the diaper area
-elderly should only use high potency in short bursts
-very high potency should be avoided in children

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73
Q

Location of application in relation to topical corticosteroids

A

thinner the skin, the lower potency it should be
medium-high to very high are needed for chronic, hyperkeratotic lesions and areas involving palms and soles

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74
Q

Indication/type of lesion in relation to topical corticosteroids

A

lower potency are best for inflammation
medium to high good for chronic lesions in thicker areas
super-potent reserved for short term use

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75
Q

Local adverse effects of topical corticosteroids

A

atrophy (occur where absorption is high, cause thinning)
telangiectasia
striae
purpura
steroid acne
hypersensitivity rxns

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76
Q

Systemic adverse effects of topical corticosteroids

A

glucocorticoid excess (cushing, hyperglycemia, growth suppression)
HPA axis suppression
Cataracts and glaucoma

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77
Q

How much to apply “fingertip method”

A

tip of finger to first index

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78
Q

Occlusive technique increases skin penetration up to 10x when giving topical corticosteroids when should you use these

A

only used under the direction of a physician

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79
Q

What does the wolffian duct system consist of

A

epididymis, vas deferens, seminal vesicles

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80
Q

What do androgens cause in adulthood for males

A

male pattern baldness
prostatic hyperplasia

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81
Q

What do androgens cause in senescence for males

A

decreased energy, muscle mass, bone density
insulin resistance, truncal obesity, increase serum levels

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82
Q

Testosterone is secreted by ______ cells of testes

A

leydig

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83
Q

Androstenedione and dehydroepiandrosterone are what kind of androgens

A

weak androgens
-they are then converted to testosterone peripherally

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84
Q

Androgen synthesis levels of 5 alpha reductase / aromatase _______ across tissues

A

differ

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85
Q

In androgen synthesis, liver metabolizes T to what two inactive metabolites

A

androsterone
etiocholanolone

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86
Q

The active metabolites of androgens are 5 alpha reductase - dihydrotestosterone (DHT) which has a high affinity for ___ and aromatase which is _________ (ET)

A

AR
estradiol

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87
Q

AR mutations what is androgen insensitivity syndrome

A

loss of function mutations
CAG repeat extension (Kennedy’s disease)

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88
Q

What are heptanoate and cyclopentyl propionate T esters

A

esters inhibit metabolism; low bioavailability; given IM; hydrolyzed to T

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89
Q

What is undecanoate T ester

A

oral, absorbed into lymphatic circulation, bypasses hepatic catabolism

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90
Q

Androgen Receptor Antagonists Flutamide MOA

A

AR blockage alone insufficient
-LH compensates
-given with GNRH analog

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91
Q

What is the common 5 alpha reductase inhibitor

A

Finasteride

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92
Q

Androgen Receptor Antagonists Spironolactone MOA

A

fluid retention, HTN
gynecomastia; given with MR antagonist

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93
Q

Definition of menopause

A

absence of a menstrual period for 12 months

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94
Q

Characteristics of menopause

A

dysfunctional uterine bleeding/irregular menstrual cycles
unpredictable fertility
increasing FSH levels

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95
Q

Systemic symptoms of menopause

A

hot flashes
insomnia / sleep disturbances
psychological symptoms

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96
Q

Local symptoms of menopause

A

Atrophic vaginitis
-vaginal dryness, burning, irritation
-lack of lubrication, dyspareunia
Urogenital atrophy
-lower urinary tract symptoms
-recurrent urinary tract infections
-urge and stress incontinence

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97
Q

Diagnosis and assessment of menopause

A

Going to have bleeding changes
symptoms consistent with menopause
increase FSH levels
women <40 they check FSH levels

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98
Q

Surgical menopause

A

removal of both ovaries before natural menopause occurs
increased vasomotor symptoms
receive E/P hormone replacement therapy

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99
Q

Women with h/o hysterectomy

A

no uterus, no periods, might experience symptoms, FSH levels could be measured if needed

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100
Q

Women using levonorgestrel IUD

A

eventually develop amenorrhea; no periods to monitor FSH levels could be measured

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101
Q

Non-drug / lifestyle recommendations for management of vasomotor symptoms

A

dress in layers of clothes
identify and decrease triggers: spicy foods, hot beverages, caffeine, alcohol

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102
Q

Drug therapy for perimenopause symptoms

A

CHC
-lower dose pill
-vaginal ring

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103
Q

Drug therapy for menopause symptoms

A

need both therapies
consider tissue-targeted therapy
OTC vaginal moisturizers
Vaginally inserted estrogen for more moderate to severe symptoms

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104
Q

Vaginal estrogen products

A

estrogen cream
estrogen vaginal tablet
estrogen vaginal ring

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105
Q

Key points of vaginal estrogen products

A

local effect
low dose estrogen
does not stimulate uterine lining
progestin is not needed
no time limit

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106
Q

Who should not receive systemic therapy in hormone therapy or hormone replacement therapy

A

women w/ h/o CHD
women w/ h/o breast cancer
women >60 yo or >10 yrs from menopause

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107
Q

Who should receive systemic therapy in hormone therapy or hormone replacement therapy

A

women w/ severe symptoms
if <60 yo w/in 10 yrs of menopause
use lowest dose
short-term and taper off in 3-5 yrs
transdermal therapy have lower risk of VTE and stroke than oral therapy

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4
5
Perfectly
108
Q

Example estrogens and progestin

A

estrogens: conjugated equine estrogens, estradiol
progestin: medroxxyprogesterone (MPA), levonorgestrel (IUD)

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109
Q

Menopause treatment for women with a uterus

A

must use combo of estrogen and progestin to decrease risk of endometrial cancer (use every day)
could use continuous E and cyclic P therapy (take P only 12-14 days)

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110
Q

Menopause treatment for women w/o a uterus

A

estrogen therapy alone every day

111
Q

What is the progestin drug that is used to induce withdrawal of bleeding

A

Provera
-help diagnose workup for amenorrhea
-may be used to treat women w/ dysfunctional bleeding

112
Q

What are the two major components of the testes and what are their functions

A

Leydig cells – testosterone is the major hormone secreted (LH)
Seminiferous tubules (lined with Sertoli cells) – sperm production (FSH)

113
Q

What are the 4 functions of testosterone

A

Development of the male reproductive structures
Male secondary sex characteristics at puberty
Maintenance of libido (sex drive) and erectile function
Required for the maturation of sperm

114
Q

Primary hypogonadism in male reproductive

A

(Presents with low to normal testosterone levels, poor or no sperm…elevated FSH & LH)
-Absence of testes
-Lack of testosterone production
-Lack of functional sperm

115
Q

Secondary hypogonadism in male reproductive

A

(Presents with LOW gonadotropins (FSH/LH)…low testosterone levels, no sperm)
-Pituitary adenomas
-Hyperprolactinemia
-Hypothyroidism

116
Q

Drug therapy for primary male hypogonadism

A

testosterone replacement therapy
-Restores virilization / masculinization
-Restores libido and sexual performance and energy
-Increase quality of life

117
Q

Monitoring for primary male hypogonadism

A

Symptom improvement
Testosterone levels – in the ~mid-normal range

118
Q

ADRs for primary male hypogonadism

A

↑BP, major CV events, VTE, ↑ risk of prostate cancer, ↑BPH symptoms

119
Q

Why is testosterone not given orally

A

1st pass metabolism causes many hepatotoxicity reactions

120
Q

What is the intranasal gel, transdermal patch, and transdermal gel for primary male hypogonadism

A

Intranasal-Natesto
Transdermal patch-Androderm
Transdermal gel-Androgel

121
Q

How to treat secondary hypogonadism if the man does not want children

A

Testosterone levels achieved in the blood do not ↑ testosterone levels in the testes that are high enough to cause the production of sperm

122
Q

How to treat secondary hypogonadism if the man wants children

A

Give “Gonadotropins” to restore virilization and spermatogenesis
The drugs are given by IM injection 3 times per week

123
Q

What are the two steps in fixing secondary hypogonadism if the man wants children

A

-Give Human Chorionic Gonadotropin (hCG) - stimulates Leydig cells to make testosterone
-Give a source of FSH - monitor sperm count; mix of FSH and LF

124
Q

What is Benign prostatic hyperplasia (BPH)

A

a benign enlargement of the prostate gland that occurs as men age

125
Q

What are the two prostate growth periods

A

Puberty through age 25-30yrs. Reaches normal size ~5-20gm
Starts again at ~40yrs through 80yrs.

126
Q

Prostate tissue: Glandular epithelial tissue composes 20-30% of BPH tissue

A

-Growth is stimulated by the androgen hormone dihydrotestosterone (DHT)
-Men with large prostates (>40-50gm) may have more epithelial tissue
-This tissue responds to 5-alpha reductase inhibitors (↓ DHT production)
-5a-reducatase inhibitors can reduce the size of the gland

127
Q

Prostate tissue: Smooth muscle tissue composes 70-80% of BPH tissue

A

-Smooth muscle tissue is less sensitive to androgen hormones
-Smooth muscle tissue growth is stimulated by other mechanisms (i.e., estrogen)
-Muscular tissue is under alpha-adrenergic tone
-This tissue responds to alpha adrenergic blocker therapy

128
Q

What is LUTS (lower urinary tract symptoms)

A

Symptoms are caused by many factors; both static (enlargement) and dynamic (muscle tone)

129
Q

What are the obstructive symptoms of LUTS

A

Hesitancy
Weak urine stream
Intermittency
Dribbling
Bladder fullness

130
Q

What are the irritative symptoms of LUTS

A

Frequency
Urgency
Urinary incontinence
Nocturia

131
Q

What are the 4 complications of BPH

A

-Urinary retention
-Recurrent urinary tract infection (UTI)
-Irreversible impairment of bladder function
-Chronic renal failure

132
Q

Assessment of BPH

A

-Medical history
-Duration and description of LUTS
-Sexual function
-Overall health / other medical conditions
*Current medications (antihistamines, decongestants, anticholinergic drugs etc.)

133
Q

BPH: Objective / Recommended initial tests for a basic evaluation (of any man w/ LUTS)

A

Urinalysis
Physical exam with Digital Rectal Exam (DRE)
PSA level
Frequency/volume charts

134
Q

What should the PSA levels be in men over 60 and then in men under 60

A

If ≥60yoPSAshouldbe<4mg/ml
If < 60yo PSA should be < 2.5 mg/ml

135
Q

What is the key point when determining LUTS

A

Serum creatinine is NOT recommended for the initial evaluation for LUTS

136
Q

Treatment of BPH non pharm “Watchful Waiting” strategy

A

patient is monitored but takes no active therapy
follow-up with patient ~12months

Appropriate for
-Mild symptoms (AUA < 8)
-Moderate symptoms (AUA 8-19) & patient is NOT bothered by them.

137
Q

Treatment of BPH non pharm lifestyle modifications to reduce symptoms

A

Fluid restriction / Fluid restriction in the evening
Decrease caffeine and alcohol consumption
Avoid drugs known to worsen symptoms

138
Q

Drug therapy for patients with BPH

A

Alpha-1 receptor antagonists (relax smooth muscle, urinary flow increased)
monitor 2-4 wks

139
Q

What are the two non-selective alpha blockers used in BPH

A

terazosin
doxazosin

140
Q

What are the three selective alpha blockers used in BPH

A

tamsulosin
silodosin
alfuzosin

141
Q

What are the non-selective alpha 1 receptor antagonists associated with

A

first dose syncope

142
Q

5 alpha-reductase inhibitors MOA

A

↓ conversion of testosterone to dihydrotestosterone (DHT)
(reduces prostate size by 25%)

143
Q

What are the use of 5 alpha-reductase inhibitors appropriate for

A

Men with enlarged prostates as evidenced by either:
-Estimated size of at least 40gm
-PSA level ≥ 1.5

144
Q

Monitoring and follow-up for 5 alpha-reductase inhibitors

A

3 months
takes 6-12 months to see new effect

145
Q

Options – similar clinical effectiveness for 5 alpha-reductase inhibitors in BPH

A

finasteride (Type II 5a-reductase inhibitor)
dutasteride (Non-selective 5a-reductase inhibitor)

146
Q

Sexual side effects of 5a-reductase inhibitor

A

↓ Libido; ejaculatory dysfunction (3-15%); erectile dysfunction (3-5%)

147
Q

Clinical monitoring concerns of 5a-reductase inhibitor

A

-Patients need a baseline PSA level before starting therapy
-5a-reductase inhibitors decrease PSA levels by 50%
-A delay in prostate cancer diagnosis has been observed if this is not remembered

148
Q

When to use surgical interventions in BPH

A

Patients with malignant or complicated disease
Patients with moderate to severe disease unresponsive to pharmacologic therapy

149
Q

Types of Sexual Dysfunction in Men

A

Decreased libido
Increased libido
Delayed ejaculation
Premature ejaculation
Retrograde ejaculation
Infertility
Erectile dysfunction

150
Q

Erectile dysfunction: hormonal classification

A

hypogonadism, hyperprolactinemia, hyper/hypothyroidism, adrenal disease

151
Q

Erectile dysfunction: neurologic classification

A

cerebral disease, stroke, spinal disease, peripheral neuropathy (diabetes)

152
Q

Erectile dysfunction: vascular classification

A

atherosclerosis, CAD, PVD, HTN, hyperlipidemia; diabetes

153
Q

Pathophysiology of ED

A

-With increasing age – collagen and elastic fibers in the penile structure decrease
-Decrease of smooth muscle content in men over 65yrs
-Decrease in sensitivity, metabolic imbalance of contractile and relaxing factors “Endothelial dysfunction”

154
Q

Physiology of penile erection

A

Erection begins with stimulation
the release of nitric oxide
↑cGMP
development of an erection

155
Q

What enzyme metabolizes cGMP

A

Phosphodiesterase (PDE)

156
Q

Oral PDE-5 Inhibitors MOA

A

Inhibition of PDE5 prevents the metabolism of cGMP
↑ cGMP levels…helps to initiate & maintain an erection

157
Q

What are the Oral Available products for PDE-5 Inhibitors

A

avanafil: 15 min before sex
sildenafil: 60 min before sex
vardenafil: 60 min before sex
TADALAFIL: 30 min before sex
(no more than 1 dose per 24 hrs)

158
Q

Oral PDE-5 Inhibitors effectiveness

A

consider a trial of 7-8 doses
If one drug does not work try another one
assess how they are using it (are they engaging in foreplay)

159
Q

Adverse effects of Oral PDE-5 Inhibitors

A

Headache, flushing, nasal congestion, heartburn
Cyanopsia
Hypotensive effects

160
Q

Contraindications of Oral PDE-5 Inhibitors

A

Contraindicated with any organic nitrate due to severe hypotension that may result
Examples: nitroglycerin, isosorbide dinitrate

161
Q

Priapism Precautions in Oral PDE-5 Inhibitors

A

-Is an erection lasting > 4hrs
-Is a medical emergency; immediate medical attention should be sought
-Penile tissue damage and permanent loss of erectile function may result

162
Q

Other treatments for erectile dysfunction

A

Alprostadil
VED- Vacuum erection device
Penile prostheses

163
Q

Hypopituitarism for male reproductive

A

-Can be due to primary pituitary disease or secondary hypothalamic disease
-Can be partial
-Can be complete “panhypopituitarism” - historically refers to loss of all anterior pituitary
hormones

164
Q

Etiology of Hypopituitarism for male reproductive

A

Tumors - pituitary tumors are the #1 cause
(Microadenoma < 10mm Macroadenoma >10mm)
Infarction of the vasculature of the gland
Trauma / Whiplash type injuries
Neurosurgery or Radiation
Autoimmune disease, Infection/Inflammation, Idiopathic

165
Q

Symptoms of Hypopituitarism for male reproductive

A

You only need about 30% of the pituitary gland to function Symptoms usually appear when ~70-80% of the gland is destroyed

166
Q

Hypopituitarism for male reproductive causes a hormone deficit of

A

GH (short stature in children, weight gain, metabolic disturbance, and fatigue in adults)
FSH/LH (hypogonadism and infertility)
TSH
ACTH
Prolactin

167
Q

Diagnosis of Hypopituitarism for male reproductive

A

History & physical
Imaging studies
Laboratory analysis
Stimulation testing

168
Q

Treatment of Hypopituitarism for male reproductive if there is an ATCH deficit

A

Give a glucocorticoid to prevent adrenal insufficiency Increase dose during states of stress, e.g., infection, surgery

169
Q

Treatment of Hypopituitarism for male reproductive if there is TSH deficit

A

levothyroxine

170
Q

Treatment of Hypopituitarism for male reproductive if there is FSH/LH deficit

A

Males: Testosterone
Females: CHC
For Fertility: Gonadotropins (Menotropins), Synthetic hCG

171
Q

Treatment of Hypopituitarism for male reproductive if there is growth hormone

A

the use of synthetic growth hormone is AGE dependent

172
Q

What are the two components of the bone

A

Minerals: provide tensile strength
Organic: proteins, bone cells

173
Q

What are the the sources of calcium

A

Absorption of Ca++ from the GI tract
Bones

174
Q

The regulation of calcium homeostasis involves what 5 things

A

Parathyroid Hormone (PTH)
1,25(OH)2 D = calcitriol
Bones
GI tract
Kidneys

175
Q

What are the two functions of the parathyroid hormone

A

-to control ionized Ca levels in a very tight range
-to do this it produces and secretes parathyroid hormone (PTH)

176
Q

The result of increased PTH causes and increase in what levels

A

Calcium

177
Q

What are three things that stimulate the increase of PTH secretion

A

The main trigger = Low Ionized Calcium Levels
Low vitamin D levels
High phosphorus levels*

178
Q

Disorders of PTH: Primary Hypoparathyroidism

A

Due to loss of function or removal of PTH gland(s)
-Will cause signs and symptoms due to hypocalcemia
-Is managed with the administration of Calcium and Vit D supplements

179
Q

Disorders of PTH: Primary Hyperparathyroidism

A

due to hyperplasia or increased activity of PTH gland
-cause signs and symptoms due to hypercalcemia
-managed with surgery

180
Q

Disorders of PTH: Secondary Hypoparathyroidism

A

Occurs when there is a primary disorder that is causing hypercalcemia

181
Q

Disorders of PTH: Secondary Hyperparathyroidism

A

-Triggered by hypocalcemia
-Triggered by low vitamin D levels (vitamin D insufficiency / deficiency)
-Triggered by hyperphosphatemia* (CKD is the most common cause)

182
Q

Vitamin D2 (ergocalciferol)

A

Diet - soy, yeast…
Fortified foods – milk, OJ, some cereals
OTC Dietary supplements
Rx products

183
Q

Vitamin D3 (cholecalciferol)

A

Diet – cod liver oil, sardines, salmon
Fortified foods – milk, OJ, some cereals
OTC Dietary supplements
Rx products
Synthesized in the skin from UVB exposure

184
Q

The first hydroxylation takes place in the LIVER Vit D2/D3 is metabolized to calcidiol (25(OH) D) what are the important points of this

A

storage form
indicates Vit D status
used to monitor therapy
physiologically inactive

185
Q

The second hydroxylation takes place in the KIDNEY 25(OH) D is converted into calcitriol (1,25(OH)2 D) what are the important points of this

A

-Calcitriol is the physiologically ACTIVE form of vitamin D
-Blood levels are kept very low and are tightly regulated
-PTH stimulates the conversion

186
Q

Primary effects of active 1,25 (OH)2 D (calcitriol) in calcium homeostasis

A

Increases absorption of Ca from the GI tract
Increases calcium and phosphate reabsorption by the kidney

187
Q

Calcitonin is secreted by the __________ cells of the thyroid gland

A

parafollicular

188
Q

What is the primary function of calcitonin

A

inhibit bone resorption by inhibiting osteoclasts

189
Q

Calcitonin salmon products MOA

A

potent inhibitor of osteoclasts

190
Q

Therapeutic uses of calcitonin salmon injections

A

Adjunct treatment in hypercalcemic crisis
Paget’s disease of the bone

191
Q

Therapeutic uses of calcitonin salmon nasal spray

A

Postmenopausal osteoporosis (only in women who are > 5yrs postmenopausal)

192
Q

Etiology of Vit D deficiency

A

-Nutritional deficiency/malnourishment
-GI procedures
-malabsorption
-lack of sun
-CKD

193
Q

Clinical Presentations of Vit D deficiency

A

Fractures
Bone pain
Muscle weakness

194
Q

Classic bone disorders associated with severe Vitamin D deficiency

A

Osteomalacia (“soft bones”) – in adults
Rickets – in children
(bones are under mineralized, most caused severe deficiency for long periods of time)

195
Q

Vit D insufficiency results in hypocalcemia which causes secondary hyperparathyroidism resulting in what

A

an increase in bone resorption to increase calcium levels in the blood
an increase in the excretion of phosphorus in the urine

196
Q

At risk populations for Vit D insufficienct

A

Elderly
Dark skinned racial groups
Living above latitude 35oN

197
Q

In Vitamin D replacement therapy 1 mcg = how many units

A

40 units

198
Q

Vitamin D replacement therapy: Drisdol

A

50,000 IU/cap
VitD2 (ergocalciferol)
Requires activation by the liver & the kidney

199
Q

Vitamin D replacement therapy: Rocaltrol

A

0.25, 0.5 mcg capsules, 1mcg/ml liquid, 1mcg/ml injection
Calcitriol 1,25(OH)2D
the active form of vitamin D

200
Q

Too little free calcium causes what and too high free calcium causes what

A
  • Too low = neuronal hyper-excitability
  • Too high = neuronal depression
201
Q

What are the three control points for calcium regulation

A

Absorption – intestines
Excretion – kidneys
Storage – bones

202
Q

What does Parathyroid Hormone (PTH) do to serum calcium and serum phosphate

A

increase calcium
decrease phosphate
(produced by chief cells)

203
Q

Osteoblast vs Osteoclast

A

Osteoblast: promotes bone formation
Osteoclast: promotes bone resorption
(PTH promotes precursor differentiation, PTH stimulates signaling)

204
Q

Calcium feedback regulation of Parathyroid Gland: PTH ↑ Serum Calcium

A

↓ Calcium Excretion
↑ Active Vitamin D Metabolites
↑ Bone Calcium Resorption

205
Q

Calcitonin are produced in C-cells of thyroid gland: ↓ serum calcium

A

↓ bone resorption
↑ renal excretion

206
Q

What are the three pharmacological effects of Calcitonin

A

-Attenuates absorptive ability of osteoclasts
-Inhibits formation of new osteoclasts
-Has weak effect in kidney and intestine

207
Q

What is converted to 25-Hydroxycholecalciferol as a precursor in the liver

A

Vitamin D3

208
Q

What is converted to 1,25-Dihydroxycholecalciferol to active form in the kidney

A

Vitamin D3

209
Q

Adverse effects of bisphosphonates

A

erosion of esophagus

210
Q

What are the Bisphosphonates drugs that : inhibit osteoclast-mediated resorption

A

-pamidronate, zeldronate IV
-alternative form raloxifene which is a selective estrogen receptor modulator

211
Q

What is cortical bone

A

it is dense and stiff, a major component of the long bones of the legs, arms

212
Q

What is trabecular bone

A

more flexible; provides shock absorption

213
Q

Defn of osteoporosis

A

a skeletal disorder of compromised bone strength which predisposes a person to ↑ fracture risk

214
Q

Establishment of optimal peak bone mass in osteoporosis

A

Genetics
Physical activity
Ca & Vit D intake
Proper endocrine function (GH, thyroid , sex hormones)

215
Q

Contributions to bone loss as we get older

A

Decreased osteoblast function
Decreased calcium intake and absorption from the gut
Decreased sun exposure ↓vitamin D production
In women…postmenopausal loss of estrogen (and in older men, loss of testosterone)

216
Q

Risk factors for low bone mass / osteoporosis

A

Genetic
Lifestyle: smoking, inactivity
Nutrition: lactose intolerance
Medical disorders / Drug therapy

217
Q

How is BMD measured? (bone mineral density)

A

DXA scan (Dual-energy X-ray Absorptiometry)
-has the best correlation with fracture risk; the gold standard test

218
Q

Where is BMD measured?

A

“Central bones” (lumbar spine or hip/femoral neck) – give the best predictor of risk
“Peripheral bones” (forearm, heel, fingers)
Less predictive of risk than central measurement; for screening purposes only

219
Q

What is T score

A

Compares patient’s BMD with the mean BMD of a healthy young person of the same gender
-represents the # of standard deviations from the mean BMD

220
Q

What is a normal t-score

A

scores > -1.0

221
Q

What is the t-score of low bone mass

A

T-score between –1.0 and –2.5

222
Q

What is the t-score in patients that have osteoporosis

A

T-score ≤ –2.5

223
Q

Recommendations for BMD measurement / monitoring: Initial Screening

A

-To identify those at risk for OP fractures – no consensus exists
-Women > 65yrs
-Men > 70yrs
(postmenopausal >50 yrs who have age-related fracture)

224
Q

Follow up and monitoring for BMD measurement

A

If T-score is normal…recheck in 5yrs
If T-score indicates Low Bone Mass, recheck in ≥ 2yrs
If T-score indicates osteoporosis, drug therapy is recommended to treat osteoporosis
If drug therapy started, recheck in 2-5yrs depending on the treatment chosen

225
Q

Dorsal kyphosis / “Dowager’s hump”

A

Loss of height
Back pain
Loss of mobility / function

226
Q

Fragility fracture defn

A

a fracture that occurs in the absence of a major trauma

227
Q

Common sites of fragility fractures

A

spine, ribs, hip, pelvis, wrist, forearm

228
Q

Common causes of fragility fractures

A

fall from standing height
bending, lifting, or twisting
coughing, sneezing

229
Q

Risk factors for falling

A

Poor health
Loss of balance
Use of sedating medications
Environmental…rugs, no bath rails, obstacles…

230
Q

Risk PREDICTORS for clinical bone FRACTURES are:

A

Low BMD
Age >65yrs
Personal history of adult fragility fracture
Family history of fragility fracture due to OP
Current cigarette smoking
Current glucocorticoid steroid use
Low BMI (underweight)
Excessive alcohol use

231
Q

What is the FRAX risk assessment tool

A

Calculates a person’s 10year risk for hip or other major OP fracture

232
Q

What are the complications of osteoporosis

A

fracture
fracture pain
loss of mobility
nursing home placement
depression
death

233
Q

Primary Osteoporosis defn

A

is due to the aging process; is not due to some other cause

234
Q

“Postmenopausal osteoporosis”

A

After the peak BMD in 20-30s, bone loss begins…it accelerates at menopause
10-25% of bone is lost in the decade after menopause; up to 15% in the first 5years
mainly loss of trabecular bone

235
Q

What can slow down postmenopausal osteoporosis

A

having enough calcium and vitamin D

236
Q

Secondary osteoporosis defn

A

is caused by or is exacerbated by other diseases or drugs

237
Q

What is the most common cause of secondary osteoporosis

A

Chronic glucocorticoid therapy

238
Q

Secondary osteoporosis should be suspected if a fracture/fragility fracture occurs

A

In pre-menopausal women
In men < 70yrs
In someone with no risk factors
Patients with multiple low trauma fractures

239
Q

What is Z score

A

-Compares patient’s BMD with the mean BMD of a control group matched for age & sex
-If the Z-score is less than –2 secondary osteoporosis should be suspected

240
Q

Strategies for prevention of osteoporosis

A

Achieve the highest peak bone mass as possible while younger
Reduce bone loss
Prevent falls
Adequate Calcium and Vit D intake

241
Q

UL of calcium

A

2,000 mg per day, increase risk for kidney stones

242
Q

Frequency of dosing practical issues related to calcium

A

as dose increases, the % of calcium absorbed decreases
single dose should not be more than 500-600 mg
typically given in divided doses, one dose at bedtime if possible

243
Q

What are the two calcium salts to use

A

calcium carbonate (Tums, needs stomach acid for absorption)
Calcium Citrate (citracal)

244
Q

Calcium drug interactions

A

tetracyclines, fluoroquinolones, bisphosphonates, levothyroxine
(need to separate the drug dose from the calcium; take 1hr before or 4hrs p Ca++)

245
Q

UL of vitamin D

A

4000 units
(should have around 800 units per day)

246
Q

Lifestyle changes to prevent osteoporosis

A

stop smoking
increase physical activity
fall prevention

247
Q

When to use bisphosphonate drugs for prevention of osteoporosis

A

T score of 1 to -2.5 AND frax >3% hip or >20% major osteoporotic

248
Q

Non drug therapy for primary osteoporosis

A

Lifestyle modifications
Adequate Calcium + Vitamin D intake

249
Q

Diagnosis of Osteoporosis

A

-T-score ≤ –2.5
-History of a fragility fracture (regardless of bone mineral density)
-Incidentally found (asymptomatic) vertebral compression fracture

250
Q

Bisphosphonates MOA

A

inhibits osteoclast activity; ↓ resorption of bone

251
Q

What are the bisphosphonates drugs that are used to treat primary osteoporosis

A

Alendronate
Risedronate
Zoledronic Acid

252
Q

Oral administration counseling points for bisphosphonates

A

at least 30 min before eating or drinking
take only with water
must be separated from other meds

253
Q

Adverse effects of bisphosphonates

A

GI, nausea, ab pain, heartburn (stay upright 30 min after taking)
Jaw
Atpyical femoral fractures

254
Q

What is the duration of ORAL bisphosphonate treatment

A

5 years

255
Q

What is Denosumab (Prolia®) is used for primary osteoporosis, what is its MOA

A

Denosumab is a monoclonal antibody with affinity for RANKL
-blocks the interaction between RANKL and
RANK

256
Q

When to use Denosumab (Prolia®)

A

Treatment of osteoporosis
Prevention of bone loss in certain patients
Treatment/prevention of of glucocorticoid-induced osteoporosis

257
Q

Effects of Denosumab

A

Increase BMD
decrease vertebral, non-vertebral and hip fractures

258
Q

Adverse effects of denosumab

A

generally, well tolerated
(atypical femoral fractures have been reported)

259
Q

What is the duration of denosumab treatment

A

5-10 years

260
Q

What is the second line therapy drugs for osteoporosis

A

Raloxifene
PTH

261
Q

Raloxifene MOA

A

it is a SERM
Agonist: Mimics effects of estrogen on bones and lipids
Antagonist: Blocks effects of estrogen in the breast & uterus

262
Q

Effects of raloxifene

A

Increase BMD spine and hip
decrease spinal fractures
effects on the bone stop when the drug is stopped

263
Q

Adverse effects of raloxifene

A

hot flashes
blood clots

264
Q

When are the parathyroid hormone drugs teriparatide and abaloparatide used

A

moderate to severe osteoporosis in postmenopausal women
men and women w/ GIOP w/ high risk of fracture (only teriparatide)
OP in men w/ hypogonadal disorders and increase risk of fracture (teriparatide)

265
Q

MOA of teriparatide and abaloparatide

A

Has anabolic activity if given once a day
Helps to build bone; increases bone density
Effects on the bone stop when the drug is stopped

266
Q

Adverse effects of teriparatide and abaloparatide

A

osteosarcoma
Do not use in pts with prior skeletal irradiation therapy
Do not use with unexplained increase in alkaline phosphatase or Paget’s disease

267
Q

Use of PTH drugs for osteoporosis are limited to ___ years

A

2

268
Q

What is the last line therapy for osteoporosis

A

Calcitonin salmon Nasal Spray
-used for treatment of OP in women who are 5 years postmenopausal
-reduce spine fractures

269
Q

Glucocorticoid Induced Osteoporosis (GIOP) background

A

The greatest bone loss is during the first 6-12 months of therapy

270
Q

Pathogenesis of Chronic Glucocorticoid exposure

A

Decreases osteoblast function by affecting the activity of IGF-1 (resulting in decreased bone formation)
Promotes hypocalcemia (increases bone resorption)

271
Q

Prevention and Treatment of Glucocorticoid Induced Osteoporosis (GIOP)

A

Use the lowest dose of steroid
Adequate Calcium + Vitamin D intake
(Elemental Calcium 1500mg and vitamin D 800 -1000 IU per day)

272
Q

Drug therapy use in Glucocorticoid Induced Osteoporosis (GIOP)

A

Bisphosphonate therapy for any patient starting prednisone >5mg daily if duration of therapy is expected to last > 3 months
Denosumab treatment for glucocorticoids at a daily dose equivalent to ≥7.5 mg of prednisone for an anticipated duration of at least 6 months
Obtain a BMD in any patient that has already received GC therapy > 6 months

273
Q

How often to repeat BMD if the patient has already received GC therapy >6 months and when should you start a bisphosphonate drug in this case

A

BMD yearly
Start bisphosphonate drug if the T-score is < -1

z S1: Module (8 decks)

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