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Therapeutics 2 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

what is healthy aging?

A

developing and maintaining functional ability that enables wellbeing in older age.

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2
Q

goals for mental health in older adults

A

prevent or treat mood disorders and cognitive impairment

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3
Q

goals for nutritional health in older adults

A

prevent or treat deficiencies; diabetes

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4
Q

goals for cognitive health in older adults

A

education, cognitively stimulating exercises, social activity

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5
Q

other goals for healthy aging?

A

stable housing, physical health, access to health care.

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6
Q

goals of care for older adults

A

maintain independence, avoid need for institutionalization, maintain quality of life, maintain functional ability

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7
Q

difference between activities of daily living and instrumental activities of daily living

A

activities of daily living: dressing, bathing, toileting, feeding, walking
instrumental: more complex; managing finances, shopping, meal prep, housekeeping, transportation, etc.

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8
Q

what psychotropic medications increase the risk of falls in older adults?

A

sedative/hypnotics, neuroleptics/antipsychotics, antidepressants, opioids

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9
Q

What other medications increase risk of falls?

A

loop diuretics, alpha blockers, sulfonylureas

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10
Q

What is polypharmacy?

A

medications without indication and medications treating ADR

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11
Q

what happens to total body water as you age?

A

decrease

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12
Q

What happens to lean body mass as you age?

A

decrease

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13
Q

What happens to body fat as you age?

A

increase; increases half-life of fat-soluble drugs

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14
Q

what happens to baroreceptor response/activity as you age?

A

decrease

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15
Q

What happens to heart rate as you age?

A

reduced variability

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16
Q

What happens to hepatic blood flow as you age?

A

decreases

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17
Q

What happens to renal blood flow as you age?

A

decreases

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18
Q

what happens to neurotransmitter volume as you age?

A

decreases ( increased sensitivity to CNS effects)

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19
Q

how does bioavailability of drugs change?

A

no change in bioavailability; slower tmax

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20
Q

what happens to vd and concentration of water-soluble drugs?

A

increased concentration bc vd is decreased

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21
Q

what happens to vd and t1/2 of lipid-soluble drugs?

A

increased vd (more fat) and increased t1/2

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22
Q

how does clearance of drugs change?

A

decreased clearance and increases half life for both hepatically and renally excreted drugs

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23
Q

reccommendations for rational prescribing

A
  • recognize new symptoms as potential ADRs
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24
Q

What do beers criteria NOT apply to?

A

palliative care/ end of life

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25
Q

most common type of UI in women?

A

urge UI (followed by stress)

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26
Q

most common type of UI in men?

A

Urge UI (followed by overflow)

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27
Q

what is overflow ui?

A

urethral blockage; bladder is unable to empty properly

28
Q

what is stress ui?

A

relaxed pelvic floor and increased abdominal pressure

29
Q

what is urge ui?

A

bladder oversensitivity; also known as overactive bladder.
characterized by urgency and frequency
may be caused by ach inhibitors

30
Q

what is stress ui caused by?

A
  • bladder pressure exceeds sphincter tone
  • can be exacerbated by alpha antagonists
31
Q

what is overflow incontinence assoc with?

A

BPH, kidney stones, or other urethral blockage; may also be neurogenic (disruption in neurologic innervation of the bladder)

32
Q

what meds cause frequency incontinence?

A

diuretics, alpha antagonists

33
Q

what meds cause urgency incontinence?

A

Ach inhibitors

34
Q

what meds cause overflow incontinence?

A

alpha antagonists, antihistamines

35
Q

first line treatment

A

non-pharm:
- scheduled/timed voiding
- pelvic floor strengthening
- avoid irritants
- absorbent products
- catheterization

36
Q

treatment for overflow:

A

non-pharm, injections or surgery, alpha antagonists

37
Q

treatment for stress:

A

non-pharm, estrogen, injections or surgery, alpha agonist

38
Q

treatment for urge:

A

non-pharm, anti-chol/anti-musc (oxybutynin, tolterodine, solifenacin), b3 agonist(myrbetriq, vibegron), injections

39
Q

treatment for neurogenic

A

non-pharm & surgery

40
Q

treatment for functional

A

non-pharm only

41
Q

anticholinergic side effects

A

can’t see can’t spit, can’t pee, can’t shit

42
Q

how long before benefit with anti-musc/anti-chol & b3 agonist?

A

2-4 weeks

43
Q

stress ui pharm options

A

duloxetine, topical estrogen, pseudofed (rare)

44
Q

Overflow ui pharm options

A

alpha adrenergic blockers (for bph) (doxazosin, tamsulosin)

45
Q

neurogenic ui

A

NO PHARM OPTIONS

46
Q

monitoring freq

A

4-8 week efficacy monitoring; consider discontinue long term

47
Q

what are platelets formed by?

A

megakaryocyte; have no nucleus

48
Q

what does contact with ecm stimulate?

A
  • platelet adhesion
  • platelet aggregation
49
Q

what is the first step of platelet activation and how?

A

glycoprotein 1a binds to collagen
gp 1b binds to von willabrand factor
= platelet adhesion!

50
Q

what regulates this process?

A

intact cells secrete PGI2 (prostacyclin) to inhibit thrombogenesis

51
Q

what is the second step of platelet activation? and how?

A

PLATELET SECRETION
- degranulation and release of ADP TXA2
and serotonin (5-HT)
= activation and recruitment of other platelets

52
Q

what is the third step of platelet activation? and how?

A

Platelet aggregation
ADP binds to other platelets; GP IIb/IIIa receptors activated and binds to fibrinogen. Platelets are cross-linked by fibrinogen.
fibrin stabilizees and anchors aggregated platelets; fibrin clot

53
Q

Aspirin MOA

A

Cox-1 inhibitor; antiplatelet drug
key: inhibition of TXA2 synthesis
prolongs bleeding time; inhibits platelet aggregation
PGI2 inhibited at TOO high of doses; no checks and balanced by tissue

54
Q

Aspirin DOA

A

36 hours

55
Q

What do COX-2 inhibitors target

A
  • prostacyclin (PGI-2) but does not target thromboxane (TXA2)
  • actually increases cardiovascular risk
56
Q

How do ADP receptor inhibitors work?

A

2 adp receptors required for activation
P2Y1 & P2Y12

57
Q

Clopidogrel MOA

A

P2Y12 ADP receptor antagonist; antiplatelet drug; plavix is a prodrug ( thienopyridine)
Works irreversibly
standard of care for MI
activated by cyp2c19

58
Q

Prasugrel MOA

A

P2Y12 ADP receptor antagonist; antiplatelet drug; prodrug
requires activation by esterases and CYP 3a4/2b6
irreversible binding; high bleeding risk

59
Q

Brilinta MOA

A

P2y12 receptor inhibitor
- reversible binding to an allosteric site
- does not require bioactivation
- fast onset
CYP 3a4 substrate; bleeding risk

60
Q

Cangrelor MOA

A

P2Y12 ADP receptor inhibitor
given IV
reversible inhibitor
no bioactivation
fast onset and short t1/2

61
Q

how do GPiib/iiia receptor inhibitors work?

A

inhibits fibrinogen crosslinking of platelets
all are given IV

62
Q

eptifibatide (integrilin) MOA

A

GPiib/iiia inhibitor; inhibits crosslinking of platelets by inhibiting fibrinogen binding. synthetic peptide; reversible; given IV

63
Q

tirofiban (aggrastat) MOA

A

GPiib/iiia inhibitor; inhibits crosslinking of platelets by inhibiting fibrinogen binding reversibly
given IV
often used with heparin in acute coronary syndrome

64
Q

Abciximab (reopro) MOA

A

monoclonal antibody; GPiib/iiia receptor inhibitor; inhibits crosslinking of platelets by inhibiting fibrinogen binding

65
Q

PDE-3 inhibitors role & drugs

A

oppose the action of P2Y12; keep platelets from being activated by ADP.
Drugs: dipyridamole, cilostazol
prevents platelet aggregation

66
Q

PAR inhibitors

A

PAR- activated by thrombin
PAR inhibitors- prevents activation of platelets by thrombin

67
Q

voxapar MOA

A

PAR-1 receptor antagonist; prevents activation of platelets by thrombin. reversible. metabolized by cyp 3a4

Therapeutics 2 (9 decks)

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