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3152 finals > contraceptives > Flashcards

contraceptives Flashcards

1
Q

a blocker eg

A
  • Alfuzosin
  • Tamsulosin
  • Silodosin

non-selective: doxazosin, terazosin, prazosin

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2
Q

prostate physiology

A

1) prostate smooth muscle maintained by noradrenaline (from adrenergic nerves)
2) Stimulate post-junctional a1-adrenoceptor
3) Prostate and LUT tissue exhibit
a) High proportion of a1A receptors

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3
Q

a1 receptor antagonist MOA

A
  • Antagonist of a1A receptor = relax smooth muscle of bladder (int. sphincter) & urethra
    ○ improve urine flow
  • Reversible antagonist
    ○ Inhibit vasoconstrict by endogenous catecholamines
    ○ Block a1-adrenoceptors on smooth muscle of
    § Prostate, prostatic urethra, bladder neck
    ○ Decr muscle tone, reduce bladder obstruction
    ○ Relax prostate smooth muscle
    ○ Improve urodynamics
    § Max urinary flow (less tension in muscle)
    § Less obstruction
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4
Q

a1 receptor antagonist reduce symptoms of

A

*Bladder instability
*Tension in smooth muscle of LUT

Improve urinary flow rate (after few hrs/ days)

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5
Q

PK of a1 receptor antagonist

A

A: well absorbed orally (0.4 mg OD)

D: highly bound to plasma proteins (90-99%)
Small Vd (0.2L/kg)

M: CYP (3A4, 2D6)
T1/2: ~10-15h

E: urine

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6
Q

ADR OF a1 receptor antagonist

A
  1. Abnormal ejaculation
  2. Backpain
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7
Q

when is a1 receptor antagonist used

A
  1. Moderate-severe symptomatic BPH regardless of prostate size
  2. Selective for a1A (prostate, blood vessels) > a1B (blood vessel, heart)
    - less effect on BP
    • LT therapy to maintain effect of urinary storage, voiding symptoms
      *Delay surgery, catheterisation
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8
Q

CI of a1 receptor antagonist

A

Concurrent use of another a1-adrenoceptor antagonist

  • prazosin, epinephrine
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9
Q

5a reductase inhibitor eg

A

Finasteride, dutasteride

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10
Q

5a reductase in normal physiology

A
  • Testosterone –> dihydrotestosterone (DHT)
    ○ Prostate to grow
    ○ Male pattern hair loss (androgenetic alopecia)
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11
Q

5a reductase inhibitor MOA

A
  • Competitive, 5a-inhibitor (no affinity for androgen receptor)
    • Inhibit conversion of Testosterone –> dihydrotestosterone (DHT)
      ○ In male external genetelia
    • Decr prostate size
      ○ Inr urine flow
      ○ Reduce freq of ACUTE retention of urine
    • Decr need for surgical procedures for prostate transurethral resection, prostatectomy
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12
Q

symptom relieve of 5a reductase inhibitor

A

inhibit 5a-reductase enzyme action
* Decr prostate size
*Incr hair growth
take up to 6mnth to see BPH clinical effect
PSA decr over time

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13
Q

PK of 5a reductase inhibitor

A

A: well absorbed orally (5mg OD)
f~0.65
No dosage adj for renal insuff/ liver failure/ elderly pt

D: highly bound to plasma proteins (90%)

M: CYP (3A4, 2D6)
T1/2: ~6h

E: 50% unchanged in feces
Metabolites in feces, urine

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14
Q

ADR of 5a reductase inhibitor

A
  1. Loss of libido, sexual potency
  2. Gynecomastia (rare)
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15
Q

clinical efficacy 5a reductase inhibitor

A

Take up to 6mnths to see BPH clinical effect after initiate

Lower dose used for male pattern baldness

Used for female hirsutism

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16
Q

CI 5a reductase inhibitor

A

Women and children
Preg

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17
Q

ED risk factors

A

alcohol
enlarged prostate BPH
psychological factors
sleep disorders
stress

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18
Q

PDE5 inhibitor

A

Tadalafil (can be used for BPH)
sildenafil, vardenafil, avanafil

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19
Q

PDE5I MOA

A
  • Inhibit phosphodiesterase type 5 (PDE5) in penis
    • Sexual stimulation, release NO
    • Incr convert GTP –> cGMP levels
      ○ Decr Ca levels
      ○ Less cGMP —> 5’ GMP (by PDE5)
  • Smooth muscle relaxation
  • Incr blood flow to corpora cavernosa
    ○Produce erection
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20
Q

PDE5 normal physiology

A
  • PDE5: highly expressed in corpora cavernosa (of penis, vasculature)
    • Poorly in myocardium
      *Tissue specificity to compound
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21
Q

PK of PDE5I

A

A: well absorbed orally (5mg OD/ PRN)
f~0.4
No dosage adj for renal insuff/ liver failure/ elderly pt
Onset 30-60min
Duration ~12h (uncomfortable)

D: widely distributed

M: CYP (3A4, 2C9 -minor) T1/2: ~4h

E: metabolites largely excreted in feces

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22
Q

ADR of PDE5i

A
  1. Headache
  2. Flushing
  3. Dyspepsia
  4. Dizzy
  5. Back pain, muscle pain (PDE11 affinity)
  6. Blur vision
    (inhibit retinal PDE6, blue-green tint of vision)

7.Priapism (prolonged erection

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23
Q

initiate PDE5i

A

Start Dose: at lowest conc
- esp for >65yrs old

1) Check for cardiac
2) Check dose
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24
Q

CI for PDE5i

A
  • Cardiac pt on GTN (nitroglycerin)
    Potentiate vasodil effect of GTN (via incr cGMP) due to incr inhibition of cGMP degradation)
  • marked vasodilation, hypotension
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25
Q

Ethinyl estradiol

A

Estrogen receptor agonist

Synthetic estrogen (birth control pills, oral contraceptives)

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26
Q

MOA of estrogen agonist

A
  • Inhibits FSH release from anterior pituitary
  • Suppress development of ovarian follicle
    * Make endometrium unsuitable for implantation of ovum
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27
Q

PK of estrogen agonist

A

A: well absorbed orally (OD)
f~0.45
IV, transdermal, TOP too
Onset 30-60min

D: highly plasma protein bound (~98% albumin)

M: metabolised by liver (T1/2 13-27hrs)

E: excreted in feces, urine

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28
Q

metabolism of estrogen agonist

A

Phase 1: EE hydroxylation (CYP3A4)

Phase 2: conjugation (to inert)
- Glucuronide(ethinylestradiol glucuronides
- sulfation (ethinylestradiol sulfate)
Enterohepatic recirc** (liver, bile, SI, ab by enterocyte, back to LIVER)

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29
Q

ADR of estrogen agonist

A

1) Breast tenderness
2) Headache
3) Fluid retention (bloat)
4) NV
5) Dizzy
6) Weight gain

  • Venous thromboembolism (VTE)
  • MI/ stroke
    *Liver damage
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30
Q

CI for estrogen agonist

A
  • History/ susceptibility to arterial/ venous thrombosis (VTE)
  • Advanced DM with vascular disease
  • Hypertension >160/100
  • Avoid breastfeeding (21 days postpartum)
  • Breast cancer women
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31
Q

indication for ethinyl estradiol

A

menopausal sx
gynecological disorders
hormone-sensitive cancers

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32
Q

progestin

A

Norethindrone

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33
Q

progestin uses

A
  • Synthetic progesterone (birth control pill, oral contraceptives)
  • treat endometriosis
  • abnormal periods of bleeding, for a normal menstrual cycle
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34
Q

progestin MOA

A
  • Inhibit luteinizing hormone release
    • Prevent ovulation
  • Make endometrium unsuitable for implantation of ovum
  • Act as progesterone receptor AGONIST
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35
Q

PK of progestin

A

A: well absorbed orally (OD)
f~64%

D: highly plasma protein bound (albumin)

M: metabolised by liver (T1/2 8hr)
Phase 1: reduction
Phase 2: conjugation (to inert)
Glucuronide
sulfation
Some % norethindrone metabolised –> EE

E: excreted in feces, urine

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36
Q

ADR of progestin

A

1) Headache
2) bloat
3) NV
4) Dizzy
5) Weight gain
6) Unpredicted spot/ bleed (initial)
7) Amenorrhea (stop)

partial conversion of norethindrone –>EE*
* Venous thromboembolism (VTE)
* MI/ stroke
* Liver damage

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37
Q

CI for progestin

A

Not for women planning preg soon after cessation of therapy

  • ovulation suppressed may persist for as long as 1.5yrs
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38
Q

structure of estrogen agonist and progestin

A

estrogen agonist
(from estrogen CH3 —-> Alkynes : allow PO)

progestin
(alter from estrogen agonist, OH –> C=O)

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39
Q

Hypertensive disorders of preg

A
  • Common causes of mortality in pregnancy
    ○ HTN: 140/90 mmHg
    § Based on >1 measurement, 4hrs apart
    § Start treatment
  • Severe HTN: >160/110 mmHg (after 2 measurements)
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40
Q

Chronic HTN

A

Preexisting HTN / New onset HTN
Before 20wks gestation

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41
Q

Gestational HTN

A

New onset HTN
w/o proteinuria after 20 wks of gestation

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42
Q

Preeclampsia

A

New onset HTN after 20 wks of gestation w/ any of new onset

1) Proteinuria
2) Sign of end organ dysfunction
3) Uteroplacental dysfunction
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43
Q

Chronic HTN with superimposed preeclampsia

A

New onset proteinuria in women with chronic HTN, no proteinuria
Before 20 wks gestation

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44
Q

Preeclampsia

A

complex multisystem disease. Not understood pathophysiology, multifactorial and varied
1) proteinuria
2) signs of end organ damage

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45
Q

Proteinuria

A
  • 24h urinary protein UTP > 300mg
  • Dipstick protein > 2 +
  • Urine protein:
    - creatinine ratio (uPCR) > 0.3 mg/dL
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46
Q

Signs of end organ damage

A
  • PLT platelet < 100
  • LFT > 2X ULN
  • Double SCr, absence of other renal disease
  • Pul oedema
  • Neurological complications **
    □ Altered mental status
    □ Visual disturbances
    □ Seizure
    □Headache
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47
Q

eclampsia

A

new onset tonic-clonic, focal, multifocal seizure superimposed on preeclampsia
§ Medical emergency –> risk to both maternal & fetal
§ Complications of eclampsia

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48
Q

Prevention of preeclampsia

A

Low dose aspirin

□ *high risk pt :  
    □ Dose: 100mg or more daily (low dose) 
    □ Started from 12-16wks. Continue till delivery
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49
Q

high risk HTN preg pt

A

HTN on previous preg
multifetal gestation (twins, triplets)
autoimmune disease
DM
CKD

50
Q

MOA of aspirin

A

□ MOA: improve utero-placenta blood flow
-Inhibit thromboxane A2, precursor of preeclampsia

51
Q

Treatment of HTN in preg

A

1) Labetalol (BB)
i. Preferred over the other BB due to less ADR on uteroplacental blood flow, fetal growth
ii. ADR: broncho-constrictive effects, bradycardia

2) Nifedipine ER (CCB)
i. Most studied, widely used CCB in preg
ii. ADR: pedal oedema, flush, headache

3) Methyldopa
i. Extensive safety data
ii. ** LOW POTENCY
iii. ADR: sedation, dizziness

4) Hydrochlorothiazide
i. 2nd, 3rd line. Potential interference with normal blood vol expansion during preg –> diuretic

5) Hydralazine
i.ADR: similar sx as severe preeclampsia –> eclampsia. NV, palpitation, flush, headache, tremor

52
Q

Contraception

A
  1. Inhibit viable sperm from coming into contact with mature ovum
    - Barriers
    - Prevent ovulation
  2. Prevent fertilised ovum from successfully implanting in endometrium
    - Unfavioural uterine environment
53
Q

Barrier techniques

(typical use) 13-21% of preg vs OHC 1-7%

A

condom (M,F)
diaphragm w/ spermicide
cervical cap

54
Q

male condom

A

CI: Allergy to latex or rubber
ADV: STD protection

DISADV:

*High user failure rate
* Poor acceptance
* Breakage possibility

55
Q

female condom

A

CI: Allergy to polyurethane
TSS
- overgrowth of staph aureus bact

ADV: STD protection. inserted ahead of time

DISADV:

*High user failure rate
* Dislike ring hanging outside vagina

56
Q

Diaphragm with spermicide/ cervical cap

A

CI:
* Allergy to latex, rubber or the spermicide
* Recurrent UTI
* Hist of TSS
*abnormal gynecologic anat

ADV: Low cost, Reusable

DISADV:

  • High user failure rate
  • Low protection against STD
  • Incr risk of UTI
  • Cervical irritation
57
Q

Hormonal contraceptives benefits

A
  • Prevent preg
  • Other health benefits
    ○ Menstrual regularity, flow, cramp
    ○ Manage perimenopause
    ○ Manage other conditions – PCOS, acne, PMS, iron-deficient anemia
    ○ Reduce risk from
    § Ovarian, endometrial cancers
    § Ovarian cysts, ectopic preg, pelvic inflamm disease, endometriosis, uterine fibroids, benign breast disease
58
Q

Combi of estrogen/ progestin
COC (combined oral contracep)

A

progestin + estrogen

59
Q

progestin MOA

A

thickens cervical mucus to
* prevent sperm penetration
* Slow tubal motility (delay sperm transport)
* Induce endometrial atrophy
* Block LH surge (prevent ovulation)

Most of contraceptive effect

60
Q

estrogen uses

A

stabilize, growth of endometrial lining, provide cycle control
Suppress FSH release

61
Q

eg of estrogen

A

○ Ethinyl estradiol (EE)
○ Estradiol valerate
○ Esterol
○ Mestranol

62
Q

dose of estrogen

A

Mod, standard 30-35
Low dose: 15-20ug
High dose: 50ug

63
Q

low dose 20-25mcg favoured for

A

○ Adolescene
○ Underweight <50kg
○ Age > 35yrs
○ Peri-menopause
○ Fewer ADR

64
Q

high dose 50 mcg favoured for

A

○ Obese, >70.5kg
○ Early-mid cycle breakthrough bleed, spotting
○ Non adherence

risk of ADR: vascular embolic events, Cancers

65
Q

CI for COC

A
  • Breast cancer
  • Ischemic stroke, MI
    (E > P)
  • Venous thromboembolism (VTE)
    • Estrogen
    • Progestins (4th gen DROS, CRYPRO, desogestrel)
66
Q

Breast cancer risk

A
  • Ok for healthy young
  • CI: >40 yrs
  • Fam hist, risk factor of BC
  • Current/ recent PMH (5yr)
  • risk incr with duration and age >40yrs
  • after discontinuation, risk returns to same lvl as those who never used COC
67
Q

Ischemic stroke, MI

A
  • ESTROGEN > PROGESTINS
  • Risk factor:
    ○ Age
    ○ HTN
    ○ Migraine with aura !!!!
    ○ Obese
    ○ Dyslipidemia
    ○ Smoke
    ○ Prothrombotic mutation
  • Change to
    ○ Prog only, barrier, low dose estrogen
68
Q

MIGRAINE WITH AURA

A

SENSORY DISTURBANCES
flashing lights, halo vision, blind spot, tingling sensation

69
Q

Venous thromboembolism (VTE)

  • Estrogen incr hepatic prod of factor VII, X, fibrinogen of coagulation cascade
  • Progestins (4th gen dros, cypro, desogestrel)
A
  • Risk factors (promote stasis)
    ○ >35yr
    ○ Obese
    ○ Smoker
    ○ cancer
    ○ Fam history
    ○ Immobilization
  • Consider change:
    ○ Low dose estrogen, older progestins
    ○ Prog only
    ○ Barrier method
70
Q

incr estrogen when

A

Breakthrough bleed early
Acne

71
Q

Reduce estrogen when

A

Bloat
NV
Breast tender, weight gain

72
Q

ADR of estrogen

A
  1. Breakthrough bleed
  2. Acne
  3. Bloat
  4. NV
  5. Headache
  6. Menstrual cramp
    a. Extended cycle, continuous, less pill free
  7. Breast tender, weight gain
73
Q

DDI of COC

A
  • Rifampicin
    • theoretical that AB alter gut flora, alter M, less active drug
    • Additional contracep (7 days) after discontinue
    • Incr dose
  • Anticonvulsants
    • Phenytoin, carbamazepine, barbiturates, topiramate, oxcarbazepine, lamotrigine
    • Reduce free serum conc of Estro, prog
  • HIV antiretrovirals
    • Ritonavir, darunavir
    • Reduce both effectiveness of COC, antiretrovirals
74
Q

absolute contraindications for COC (12)

A
  • current breast CA/ recent hist in 5yrs
  • hist of DVT/PE, acute, pts with & on anticoagulant therapy
  • thrombogenic mutations
  • major surg with prolonged immobilisation
  • current/ hist of IHD
  • HTN with vascular disease
  • HTN > 160/100 mmHg
  • cardiomyopathy
  • <21 days post partum
  • hist of cerebrovascular disease
  • migraine with aura
  • smoke >15sticks/ days & age > 35 yo
75
Q

progestin activity

A
  • Vary in pregestational activity
  • Androgenic effects
    • Androgen-to-progesterone activity ratio
    • Acne, oily skin, hirsutism
  • Pregestational activity prevent
    • late cycle breakthrough bleeding
      *Painful menstrual cramps
  • CI: BREAST CANCER
76
Q

Progestin 4th

A

Cyproterone
drospirenone

77
Q

drospirenone

A
  • Spironolactone analogue, anti androgenic action, diuretic (less bloat) , less acne

Hyperkalemia
Thromboembolism
Bone loss

78
Q

Cyproterone

A
  • Anti-androgenic, antigonadotrophic
  • Treat excessive androgen related conditions (severe acne, hirsutism)
  • not solely as contraceptive

Thromboembolism

79
Q

POP – norethisterone

A
  • Good for breastfeed, those that cannot take estrogen (NV)/ conditions that preclude estrogen

CI: current/ recent hx of breast cancer

80
Q

POP initiate

A
  • 28 active pills
  • Continuous
    ○ Start: within 5d of menstrual cycle (no need backup)
  • Any other day: back up 2 d
  • late dose > 3hr = BACK UP 2 DAYS
81
Q

Incr progestin when

A
  • Late breakthrough bleed
  • Menstrual cramp
  • Bloat (drospi – mild diuretic)
82
Q

change progestin to COC

A
  • Acne (less androgenic)
    Stop POP –> COC
83
Q

decr progestin when

A

Breast tender, weight gain

84
Q

Monophasic COC

A

Same amt of estrogen & progestin in every pill

Less confusing
Less complicated missed dose instruction

85
Q

Multiphasic COC

A

Variable amt of estrogen and progestin
4 phases (higher estrogen at start, higher prog at end)

  • Less overall prog
  • Less ADR
  • Mimics physiologic menstrual cycle

but expensive

86
Q

Conventional cycle COC schedule

A

21 days active pill
7 day placebo
= 28 days

24 days active pill
4 day placebo
= 28 days

87
Q

Extended cycle/ continuous COC schedule

A

84 days
7days placebo
0 placebo (continuous)

88
Q

Conventional cycle COC ADV

A

Period triggered when pill stop
Shorter pill free interval
- Reduce hormone fluctuation b. cycle (less SE

89
Q

Extended cycle/ continuous COC ADV, DISADV

A

Convenient
Less periods

DISADV: breakthrough bleeding

90
Q

3 ways initiate COC

A
  • 1st day of menstrual cycle
    ○ No need backup contraceptives
    ○ First 5-6 days not likely to get preg
  • Sunday start after menstrual cycle begins
    ○ Backup for 7 days
    ○ So that weekends free of menstrual periods
  • Quick start, any day
    ○ Backup for 7 days// until next menstrual cycle begins
91
Q

factors to select COC

A

hormone content required
convenience
adherence lvl
tendency for oily skin, acne, hirsutism
medical conditions (PMS)

92
Q

Hormonal content required

A

○ More/ less estrogen
§ (pt weight, adherence, early bleed)
○ More prog
§ Late bleeding

93
Q

Convenience

A

No periods? Placebo?

94
Q

Adherence level

A

Low = Higher estrogen
Monophasic

95
Q

Tendency for oily skin, acne hirsutism

A

Less prog (androgenic ADR)

change to 4th gen

96
Q

Medical conditions like PMS, dysmenorrhea (how to counter)

A

PMS (incr prog)
Dysmenorrhea (extended cycle 84 days active)
- decr hormone free interval

97
Q

ADR for COC SHOULD ….

A

Persevere on COC for 2-3 mnths

  • Usually 3-4 cycles of cycle before stabilsie
  • Unless serious ADR
    - VTE, stroke, migraine with aura, MI
98
Q

MISSED DOSE: 1 dose missed (less than 48hrs)

A

1) Take pill immediate
2) Continue rest as usal
– 2 pills on same day

No additional contraceptives required

99
Q

2 or more consecutive dose missed (more than 48hrs)

A

1) Take missed dose immediate
2) Discard rest of missed dose
3) Continue rest as usual
– (2 pill on same day)
Backup contraceptive required for 1 week

100
Q

Pills missed on last week of hormonal tablet (day 15-21)

A

1) Finish remaining active pills in current pack
2) SKIP hormone free interval
– Treat missed dose as the hormone free period
3) Start new pack next day
Backup contraceptive required for 1 week

101
Q

dont want period coming in the next week

A

Ignore placebo pills, start new pack of active pill to delay period

Continue as per usual until next placebo pill (skip 1 menstrual cycle)

102
Q

COC also available in:

A

1) Transdermal contraceptives

2) Vaginal rings

103
Q

transdermal contraceptives

A

○ Both estrogen and progestin component
○ Failure rate ~ 7% (COC)
○ Applied once wkly for 3wks – 1 patch free week
§ Not effective in pts weighing > 90kg

○ SE: similar to COC + application side rxn

104
Q

vaginal ring

A

○ Both estrogen and progestin component
○ Failure rate ~ 7% (COC)
○ Used for 3wks then discarded – 1wk free
§ Unlike diaphragms/ cervical caps
§ No need precise placement as hormones are absorbed (less user error)

○ SE: similar to COC + risk expulsion

105
Q

transdermal patch/ ring

A

continuous, higher exposure to estrogen –> risk of VTE

106
Q

Other progestin only contraceptives

A

1) prog inj
2) LARC – IUD, implants

107
Q

Progestin inj

A

○ Depot-Provera (medroxyprogesterone 1st gen), IM inj every 12wks
Good for adherence issues, need regular doctor visit
§ Good for postpartum, not to get preg soon after giving birth
§ Incr breastmilk

Failure rate ~ 4% «<(COC)

108
Q

ADR, CI of prog inj

A

○ ADR: return to fertility delayed. Depot, need to wait for the progestin to be released
§ Variable breakthrough bleeding (first 9mnths)
§ Amenorrhea after 12mnths –> 2yrs
§ Weight gain
§ Short term bone loss (Bone mineral density decr)

○ CI:
§ Avoid in older women
§ Avoid in osteoporosis risk factors, LT steroid use
§>2 yrs use, evaluate other options (bone loss incr with duration of use)

109
Q

2) Long acting reversible contraception (LARC)
Intrauterine devices IUD, implants MOA

A

1) Inhibit sperm migration
2) Damage ovum
3) Damage/ disrupt transport of fertilised ovum
4) w/ progestin (thicken mucus, endometrial suppression)

110
Q

2 types of IUD

A

LEVONORGESTREL (2nd) IUD
* Cause decr flow, ideal for menorrhagia
* 5 years

COPPER IUD
* Cause heavier menses, ideal for amenorrhea
* 10yrs
*Emergency use

111
Q

IUD CI in

A

○ Preg
○ Current STI
○ Undiagnosed vaginal bleeding
○ Malignancy of genital tract
○ Uterine anomalies
○ Uterine fibroids

112
Q

IUD adv

A

○ Typical use = perfect use (need to be inserted)
○ Effects reversible quickly after removal

113
Q

IUD disadv

A
  • Invasiveness
  • Uterine perforation
  • Expulsion
  • Pelvic infection
114
Q

LARC: subdermal progestin implants

A

4cm long implant.
68mg of etonogestrel (3rd)

used for 3yrs

115
Q

LARC: subdermal progestin implants ADR

A
  • Irregular bleeding pattern (continued use)
  • Amenorrhea
  • Prolonged bleeding
  • Spotting
  • Freq bleeding
116
Q

breakthrough bleed

A

early/mid = incr estrogen

late = incr progestin

117
Q

acne

A

less androgenic prog

incr estrogen

POP –> COC

118
Q

BLOAT

A

reduce estrogen

change to prog, mild diuretic effect (4th drospirenone)

119
Q

NV

A

reduce estrogen
take at night
change to POP

120
Q

headache

A

exclude migraine with aura
usually in pill-free week –> extended/continuous/ shorter pill free interval

121
Q

menstrual cramps

A

incr progestins
switch to extended cycle/ continuous

122
Q

breast tender/ weight gain

A

keep both estrogen, prog LOW

3152 finals (9 decks)

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