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P&T Final

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waveurflag's version from 2017-12-14 15:36

Section 1

Question Answer
TRH released fromhypothalamus
TSH released fromanterior pituitary
conversion of T4 to T3 bytissue deiodinase
Serum TSHGolden standard for diagnosis
TSHR-SAbAntibody that detects hyperthyroidism
Hashimoto's hypo
Graves'hyper
LevothyroxineSynthroid, unithroid, levoxyl
Dose for Levothyroxine1.6 mcg/kg/day (obese use IBW)
IV dosing50% of normal dose
Myxedema comauncontrolled hypothyroidism. Treat with 300-500 mcg LT4 IV loading dose
Beta Blockers non selective, propanolol, nadolol
IodideLugol's solution, do NOT use before radioactive iodine treatment
PTUPropylthiouracil, use three times a day. Preferred in 1st trimester of pregnancy. BBW: HEPATOTOXICITY
MMIMethimazole, once a day. Better safety profile.
Ophthalmopathygive prednisone after radioactive iodine treatment
Thyroid stormsevere thyrotoxicosis, treat with large doses of PTU (500-1000mg load), short acting beta blocker (IV esmolol), APAP for fever, or IV hydrocortisone
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Section 2

Question Answer
Amenorrhea can be caused byhyperprolactinemia, PCOS, or primary ovarian insufficiency.
Menorrhagia can be caused byunderlying bleeding disorders, aka von Willebrand's disease, hypothyroidism, etc.
Dysmenorrhea can be caused byrelease of prostaglandin and leukotrienes (cramps), secondary would be underlying causes
PCOS can be caused byandroogen excess, genetics, hypersecretion of LH and GnRH
PMS & PMDD can be caused byExact etiology is unknown, but may be related to low GABA and serotonin levels in the follicular phase
Progesterone Challenge Testo Used to confirm functional anatomy and adequate estrogenization  Induces withdrawal bleeding in women with secondary amenorrhea. If withdrawal bleeding does not occur, that indicates low estrogen or problem with outflow.
Hyperprolactinemia Treatment Bromocriptine and cabergoline. Both are dopamine receptor agonists, and suppress prolactin production to ensure normal levels of FSH & LH. NOT FOR CARDIAC PATIENTS
Menorrhagia TreatmentIf contraception is desired, then use HT: Exogenous estrogen + progesterone (i.e. combined oral contraceptives). If NOT, then use NSAIDS. If they are NOT effective, consider tranexamic acid
Tranexamic Acid (Lysteda™)Treats heavy menustrual bleeding by preventing fibrin degradation. Do NOT use if you have a history of THROMBOEMBOLISM
Dysmenorrhea Treatment Consider non-pharmacologic interventions. If NOT effective, use NSAIDs for cramps. If contraception is desired, consider injectable MPA or IUD
PCOS TreatmentIf pregnancy is an immediate goal, use clomiphene citrate for PCOS with an insulin sensitizing agent. If NOT, then use an insulin sensitizing agent with an oral contraceptive containg progesterone
PMS Treatment Start non-pharmacologic interventions for 2 months while the patient charts her symptoms, use vitamin B6 or calcium carbonate. If that is NOT effective, use serotonergic agents such as citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, or venlafaxine which is an SNRI.
PMDD Treatment Monophasic or continuous cycle(more preferred) hormonal contraception improves premenstrual symptoms in patients. If NOT effective, use leuprolide
Leuprolide (Lupron Depot®)Used for: endometriosis, fibroids, prostate cancer, CPP, and PMDD. The side effects are hypoestrogenic (similar to symptoms of menopause), such as HOT FLASHES
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Section 3

Question Answer
Initiation Osteocytes signal osteoblasts
Activation Osteoblasts release RANKL, which binds to RANK on osteoclasts
ResorptionOsteoclasts breakdown bone
ReversalOsteoblasts release OPG to stop RANKL, thus stopping resorption
FormationOsteoblasts increase collagen and mineralization of bone
Quiescence rest until remodeling cycle
Bone Mineral Density (BMD)Used to establish or confirm a diagnosis of osteoporosis, predict fracture risk, and monitor patients. Osteoporosis can ALSO be diagnosed by occurrence of an adulthood hip or vertebral fracture in the absence of major trauma.
Dual-Energy X-ray Absorptiometry (DXA) Central is better than peripheral.
Central DXA  The gold standard for measuring BMD  High precision, short scan times  BMD measurements of lumbar spine, proximal femur, total hip  The lowest BMD measurement is used for diagnosis. ALL women >65 and men >70 must test BMD, or younger postmenopausal women with risks, or men 50-69 yo with fracture risks
Fracture Risk Algorithm (FRAX®) • A risk assessment tool • Developed to calculate the percent probability of a hip fracture and a major osteoporotic fracture (defined as clinical vertebral, hip, forearm or proximal humerus fracture) in the next 10 years • Intended for postmenopausal women and men age 50 and older • Not validated in patients currently or previously treated with pharmacotherapy for osteoporosis • Can be used with or without data on bone mineral density (BMD)
T-Score Values BMD is expressed as a relationship to the norm and is converted into a T-score and/or a Z-score. T score compares BMD to a younger, sex matched population. Z score compares it with age matched, and sex matched population
Low Bone mass T-Scorebetween -1.0 and -2.5. Below -2.5 means osteoporosis
First Line Therapies: Bisphosphonates (ZARD) Zoledronic Acid (IV), Alendronate, Risendronate, and Denosumab (INJECTION BY PCP).
Alternate Therapies (RITA)Raloxifene (CAUSES VENOUS THROMBOEMBOLISM), Ibandronate, Teriparatide and Abaloparatide (both PENS)
Last Line Therapy (Calcitonin)Two types: Miacalcin (INJECTION) and Fortical (NASAL SPRAY). Both have a possible increased risk of MALIGNANCY.
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Section 4

Question Answer
Menopauseo Typically defined by 12 consecutive months of amenorrhea o In women who have undergone hysterectomy, symptoms define menopause o Age: about 51 years of age is the onset
Perimenopause time period preceding menopause during which fertility wanes and menstrual cycle irregularity increases o Mean duration of 4 years o Precedes the final menses by 2-8 years
Menopause Treatment: Vulvovaginal Symptoms ONLYNon-pharmacologic strategies • Pelvic floor physical therapy • Non-hormonal vaginal lubricants and moisturizers (many options available OTC)
Menopause Treatment: BOTH Vasomotor and Vulvovaginal Symptoms If patient had a HYSTERECTOMY, give Estrogen ALONE. If uterus is intact, give Estrogen-Progesterone Therapy (EPT). Continous combined is commonly used in oral, transdermal, or estrogen + IUD. Risk of VENOUS THROMBOEMBOLISM and ENDOMETRIAL CANCER.
Menopause Treatment: Vasomotor Symptoms ONLYSSRIs and SNRIs: Paroxetine, Escitalopram, Citalopram, Venlafaxine, Desvenlafaxine. Gabapentinoids such as Gabapentin and Pregabalin work well for VMS. Clonidine works for VMS, but can cause REBOUND HYPERTENSION, not preferred.
Ospemifene (Osphena®) Treats moderate to severe dyspareunia due to menopause. Risk of VENOUS THROMBOEMBOLISM, and causes HOT FLASHES
Prasterone (Intrarosa®) Approved by FDA in Nov 2016. It's the first product containing DHEA. Treats moderate to severe dyspareunia due to menopause
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Section 5

Question Answer
What is BPHNon-malignant growth of the prostate which leads to lower urinary tract symptoms (LUTS) and bladder outflow obstruction
Two types of prostate tissue Epithelial and Stromal
5 alpha reductaseenzyme that activates testosterone to dihydrotestosterone, causing prostate tissue growth
Alpha 1 ReceptorsWhen activated, causes contraction & constriction in BOTH stromal and epithelial tissue.
Detrusor Muscle Contraction occurs with activation of muscarinic receptors with acetylcholine
Medications that worsen BPH Symptoms• Androgens (testosterone) • α-adrenergic agonists (pseudoephedrine) • anticholinergics (antihistamines, TCAs) • Diuretics
Obstructive Voiding SymptomsSign of early disease. o Urinary hesitancy o Weak urinary stream o Straining to void o Incomplete bladder emptying o Dribbling o Intermittency
Irritative Voiding SymptomsSign of late disease. o Urinary frequency o Nocturia o Dysuria o Urgency (Incontinence)
Labs BUN and SCr may be INcreased
Goal: Reduce AUA symptoms score minimum of3 points
α-adrenergic antagonists (prostate <30g)Terazosin & Doxazosin (non-selective, lowers HTN), Tamsulosin, Silodosin, & Alfuzosin (uroselective has lower CV risks)
5α-reductase inhibitors (prostate > 30 g)Finasteride & Dutasteride (onset is longer, 3-6 mo). More ED complications, but works better in reducing SIZE of prostate.
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Section 6

Question Answer
Erectile dysfunction (ED)Inability to achieve or maintain an erection sufficient for intercourse
acetylcholine (ACh)increases parasympathetic activity in the penis
corpora cavernosa Composed of interconnected sinuses which can fill with blood to produce erection
Organic EDvascular, neurologic, and/or hormonal abnormalities causing ED (80%)
Psychogenic EDpatient does not respond to psychological arousal (20%)
Diabetes 50% have ED
Medications that cause ED symptoms antihypertensives & 5 alpha reductase inhibitors (such as finasteride and dutasteride)
Assess cardiovascular risk to determine if sexual activity is safe:o Sexual activity increases physical exertion, which may increase risk of MI o ED may itself be a symptom of cardiovascular (CV) disease
Psychogenic ED Treatmentpsychotherapy (ideal if partner attends as well)
PDE-5 inhibitorsSill requires sexual stimulation. ADRs are all eye related, myalgias, and hearing loss
Do NOT give PDE-5 inhibitors withCYP3A4 Substrates & alpha adrenergic antagonists (all the -zosins): increased risk of hypotension
ViagraSildenafil, quickest onset, delayed by high fat meal
Levitra, StaxynVardenafil, Levitra (not Staxyn) delayed by high fat meal
CialisTadalafil, best option. Works with BPH as well. Duration: up to 36 hours
StendraAvanafil
Alprostadilintrauethral/intracavernosal injection
Other treatmentstestosterone, vacuum erection devices,
Prosthesissimi rigid malleable rod, inflatable rod
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Section 7

Question Answer
Most common type of UIStress Urinary Incontinence
When bladder is ready to empty, detrusor muscle contracts with muscarinic stimulation by acetylcholine
Overactive bladder (OAB) Detrusor contractions are overactive
Stress urinary incontinence (SUI)Weak bladder neck and weak urethral sphincter
Overflow UIBladder outlet obstruction, detrusor underactivity and/or urethral sphincter overactivity causes urine to build up, leading to leakage
Functional UIInability to reach toilet in time due to mobility conditions
Non-pharmacologic interventiono Avoid exacerbating drugs o Toilet scheduling o Pelvic floor exercises o Weight reduction o Absorbent products o Caffeine reduction and fluid management
Treatment for OAB Anti-muscarinic/Anti-cholinergic agents (oxybutynin, tolterodine, fesoterodine, trospium solifenacin,darifenacin). β3-Adrenergic Agonists such as Mirabegron also work for OAB.
Treatment of SUIEstrogens, α-adrenergic receptor agonists (SUDAFED), and SNRIs (Duloxetine is most used)
Treatment of Overflow Incontinence Treat the underlying cause first, then use a cholinergic agent (Bethanecol).
If all other methods failConsider a catheter.
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