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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
most common type of UI in women?
urge UI (followed by stress)
26
most common type of UI in men?
Urge UI (followed by overflow)
27
what is overflow ui?
urethral blockage; bladder is unable to empty properly
28
what is stress ui?
relaxed pelvic floor and increased abdominal pressure
29
what is urge ui?
bladder oversensitivity; also known as overactive bladder. characterized by urgency and frequency may be caused by ach inhibitors
30
what is stress ui caused by?
- bladder pressure exceeds sphincter tone - can be exacerbated by alpha antagonists
31
what is overflow incontinence assoc with?
BPH, kidney stones, or other urethral blockage; may also be neurogenic (disruption in neurologic innervation of the bladder)
32
what meds cause frequency incontinence?
diuretics, alpha antagonists
33
what meds cause urgency incontinence?
Ach inhibitors
34
what meds cause overflow incontinence?
alpha antagonists, antihistamines
35
first line treatment
non-pharm: - scheduled/timed voiding - pelvic floor strengthening - avoid irritants - absorbent products - catheterization
36
treatment for overflow:
non-pharm, injections or surgery, alpha antagonists
37
treatment for stress:
non-pharm, estrogen, injections or surgery, alpha agonist
38
treatment for urge:
non-pharm, anti-chol/anti-musc (oxybutynin, tolterodine, solifenacin), b3 agonist(myrbetriq, vibegron), injections
39
treatment for neurogenic
non-pharm & surgery
40
treatment for functional
non-pharm only
41
anticholinergic side effects
can't see can't spit, can't pee, can't shit
42
how long before benefit with anti-musc/anti-chol & b3 agonist?
2-4 weeks
43
stress ui pharm options
duloxetine, topical estrogen, pseudofed (rare)
44
Overflow ui pharm options
alpha adrenergic blockers (for bph) (doxazosin, tamsulosin)
45
neurogenic ui
NO PHARM OPTIONS
46
monitoring freq
4-8 week efficacy monitoring; consider discontinue long term
47
what are platelets formed by?
megakaryocyte; have no nucleus
48
what does contact with ecm stimulate?
- platelet adhesion - platelet aggregation
49
what is the first step of platelet activation and how?
glycoprotein 1a binds to collagen gp 1b binds to von willabrand factor = platelet adhesion!
50
what regulates this process?
intact cells secrete PGI2 (prostacyclin) to inhibit thrombogenesis
51
what is the second step of platelet activation? and how?
PLATELET SECRETION - degranulation and release of ADP TXA2 and serotonin (5-HT) = activation and recruitment of other platelets
52
what is the third step of platelet activation? and how?
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
Aspirin MOA
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
Aspirin DOA
36 hours
55
What do COX-2 inhibitors target
- prostacyclin (PGI-2) but does not target thromboxane (TXA2) - actually increases cardiovascular risk
56
How do ADP receptor inhibitors work?
2 adp receptors required for activation P2Y1 & P2Y12
57
Clopidogrel MOA
P2Y12 ADP receptor antagonist; antiplatelet drug; plavix is a prodrug ( thienopyridine) Works irreversibly standard of care for MI activated by cyp2c19
58
Prasugrel MOA
P2Y12 ADP receptor antagonist; antiplatelet drug; prodrug requires activation by esterases and CYP 3a4/2b6 irreversible binding; high bleeding risk
59
Brilinta MOA
P2y12 receptor inhibitor - reversible binding to an allosteric site - does not require bioactivation - fast onset CYP 3a4 substrate; bleeding risk
60
Cangrelor MOA
P2Y12 ADP receptor inhibitor given IV reversible inhibitor no bioactivation fast onset and short t1/2
61
how do GPiib/iiia receptor inhibitors work?
inhibits fibrinogen crosslinking of platelets all are given IV
62
eptifibatide (integrilin) MOA
GPiib/iiia inhibitor; inhibits crosslinking of platelets by inhibiting fibrinogen binding. synthetic peptide; reversible; given IV
63
tirofiban (aggrastat) MOA
GPiib/iiia inhibitor; inhibits crosslinking of platelets by inhibiting fibrinogen binding reversibly given IV often used with heparin in acute coronary syndrome
64
Abciximab (reopro) MOA
monoclonal antibody; GPiib/iiia receptor inhibitor; inhibits crosslinking of platelets by inhibiting fibrinogen binding
65
PDE-3 inhibitors role & drugs
oppose the action of P2Y12; keep platelets from being activated by ADP. Drugs: dipyridamole, cilostazol prevents platelet aggregation
66
PAR inhibitors
PAR- activated by thrombin PAR inhibitors- prevents activation of platelets by thrombin
67
voxapar MOA
PAR-1 receptor antagonist; prevents activation of platelets by thrombin. reversible. metabolized by cyp 3a4

Therapeutics 2 (9 decks)

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