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Pharm > T3 > Flashcards

T3 Flashcards

1
Q

phenylephrine

A

selective a1 rec
raises BP like NE–>more ref. brady
correct neurogenic shock, use during therap. spinal and other anesthesia
do not stimulate heart

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2
Q

phenyephrine local uses

A

hemorrhoids
nasal congestion
mydriatic agent
supraventricular tachycardias (IV)

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3
Q

midodrine

A

newer than phenyleprine
prodrug, “smoother absorbtion”
othostatic hypotension, urinary incontinence
–counterindicated for HTN pts.

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4
Q

oral absorption of phenylephrine is..

A

poor, midodrine is better

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5
Q

cocaine

A

inhibits reuptake of NE at symp. nerve terminals

  • good LOCAL anesthetic, topical, local mucous membranes and for intubation of trachea through the nose
  • constricts BVs at site, drug stays at site
  • rarely for pain relief and redusing epistaxis while nose intubation
  • CNS effects: abuse
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6
Q

psuedoephiedrine and ephedrine

A

stimulate rel. of NE from symp. nerve endings independent of nerve APs
–>stim. adrenergic rec. directly

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7
Q

psuedoephiedrine and ephedrine tx

A

nasal and bronchial congestion–>promotes nasal and sinus drainage

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8
Q

amphetamine, methamphetamine, methylphenidate

A

stim. rel. of catechols from symp. and central nerve endings

- concern is central effects

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9
Q

pharmkin considerations: selective a1, B2, B3 direct acting agonists and ind. acting drugs

A

readily absorb, tx effective after oral admin, action last for hours

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10
Q

pharmkin considerations: cocaine (and some other direct-acting agonists: NE, E, Isoproterenol, DA, Dobutamine))

A

must be given parenterally(IV, inhalation) to be effective tx and actions last only few min if given IV
*last longer if whole tissue injection: oral mucosa, skel. musc

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11
Q

tolerance in sympathomimetic drugs

A

recepters down regulate when exposed chronically
ex: DA or dobutamine for CHF pts., chronic nasal congestions w. pseudoephed., bronchoconstr in asthmatics w. sel B2 agonists (oral typ worse than inhaled)

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12
Q

rebound phenomena

A

symptoms you were attempting to tx return “with a vengeance”

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13
Q

side effects of symp. agonists

A

gen. extension of tx effects
lack of suff. rec. selectivity
CNS side effects
*worse when dose is higher

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14
Q

sympathomimetic side effects examples

A

tx dep. cardiac contractility after MI w. B agonist–>stim B rec.–>lead to more O2 deficite, tachy, arrhy

  • attempt to prevent hypotension w/ NE–>HTN
  • local dermal tiss. necr. when IV inf of a agonist for systemic tx ends up in surrounding tissue
  • tx urine incontinence/ortho. hypotension w/ midodrine–>a-1 mediated piloerection and bladder urine retention
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15
Q

symp. drugs SE: lack of suff. rec selectivity

A
  • attempt to prev. premature labor w/ terbutaline (B2 rec) ending up w/ tachy in both mother and fetus (all cardiac B rec)
  • inha. albuterol for asthma–>B2s AND B1 stim–>arrhythmias
  • DA to inc. renal blood flow–>went to high–>stim. a1 rec–>offset vasodilation
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16
Q

side effects: CNS

A

mainly seen w. indirect acting sympathomimetics (dir. less likely to enter brain, exc: nervousness from epinephrine (pt. “sensing” drug, not nec. CNS effect)
i.e. insomnia, anxiety, convulsions, agitation, hallucinations, etc)

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17
Q

B-Blockers

A

Acebutolol (Sectral)
Atenolol (Tenormin)
Exmolol (Brevibloc)

Metoprolol (Lopressor, Toprol-XL)
Nadolol* (Corgard)

Pindolol*
Propranolol* (Inderal-LA)
Timolol* (Timoptic)
*B1 AND B2 rec selectivity
ALL inhib B1
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18
Q

intrinsic sympathomimetic action (ISA) of B blockers

A

partial agonist effect
*can never deliver so much drug to completely shut down receptors
(in general: rev. competitive antagonists)

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19
Q

B blockers partial agonists

A

Acebutolol

Pindolol

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20
Q

B blockers membrane stability (“local anesthetic” action)

A

acebutolol
metoprolol?
pindolol?
propranolol

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21
Q

B blocker lipid solubility

A

L: others
M: metoprolol, pindolol
H: propanolol
-low: no liver inactivation but direct excretion thru kidney EXCEPT Esmolol: Low, but inactivated by circulating esterases (short duration)
-high: more likely to enter brain and be cleared by liver

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22
Q

B blockers: B1

A

by inhib. B1 rec: all B blockers can dec. most symp. supported cardiac fund (dec. HR, contract, automat, conduction velocity)

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23
Q

antiangina use of B blockers

A

–>by dec. HR and contract, can dec myocardial O2 deficit that causes angina inputs w/ poor coronary O2 deliver (atheroscl)

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24
Q

B blocker: anti-HTN

A

lower HTN by dec. rate and contractility, also dec renin sec (B1) in kidney JG cells

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25
Q

B blocker: prevent post-MI arrhythmias

A

dec. automaticity in potential cardiac pacemaker cells (in extraneous (non-SA) pacemaker cells)
- slow/inhibit automaticity (AV node, purkinje rec, wall of ventricles) can slow down conduction thru ventricles: prevent supraventricular arrythmias

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26
Q

B blockers: protect heart from

A

dangerous catecholamine-ind. tachys and arrhythmias during:

  • surg. removal of pheochromocytomas (NE, E release)
  • “thyroid storm” in hyperthyroidism: exc. catecholamine ACTION (not nec. presence) in heart
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27
Q

what about B2 blockers??

A

do not want to inhibit vasodilation, alpha rec. would then be uninhibited–>vasoconstrictor

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28
Q

B2 blockers

A
  • tx for glaucoma: dec. AH production in ciliary epithelium to lower IOP
  • timolol (Timoptic): no membrane stabilizing, unless v. high dose (“local anesthetic action”, good!) if - undesirable in eye–>could lead to eye damage

what about Nadalol? (non mem stab, B2) -low lipid solubility, would need systemic dose

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29
Q

unlike nonsel. B blockers w.out ISA (partial agonist activity), those WITH ISA (pindolol) do not interfere w.

A

B2-mediated relaxation of vessels in skeletal muscles
–>can actually enhance such relaxation enough to dec. TPR–>overall antiHTN mech (“vasodilator” B-blockers), further enhancement of lowering BP

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30
Q

membrane stabilization may have..

A

antiarrhythmic props. but at such high doses, not commonly used (propranolol)

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31
Q

high Lipid solubility

A

may enter brain: potentially beneficial CNS-rel. CV actions (lowering BP)
-inactivated by liver, req. good liver fund.

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32
Q

low lipid solubility

A

req. good RENAL function–>inactivated by renal excr.

* lipid sol. det. drug choice for certain pts.

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33
Q

this drug has shortest duration due to rapid inactivation by circ. esterases (10 min)

A

Esmolol: used only IV to control critical, acute CV conditions (HTN, MI, SV arrhythmia post-surg) want only temporarily

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34
Q

longer acting B blocker (24 hr duration)

A

Nadolol: for chronic conditions where pt. compliance is important

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35
Q

other nonspecific actions of B blockers

A
  • migraine and “stage fright”

- heart failure?? (CI!: not well understood but true)

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36
Q

B1 blocker side effects: excess depression of cardiac B1 rec

A

sinus brady, AV blockade, depressed CO–>Raynaud’s and intermittent claudication, exercise intolerance (phys. active pts)

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37
Q

B2 blocker side effects

A
  • bronchoconstriction (or spasm) in asthmatics due to inhib. of B2 med. relax. of airways
  • intermittent claudication and exer. intolerance (no B2 vasodilation)
  • delayed recovery from insulin-induced hypoglycemic episodes (dec. B2 med hep. glucose output)
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38
Q

partial agonist activity B blockers

A

potentially same side effects but less severe (understandably w/ agonist activity)

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39
Q

lipid solubility side effects

A

inc. CNS effects: i.e. somnolence, depression

40
Q

other non-sp. B blocker side effects

A
  • aggravation of insulin resistant states in HTN and T2 DM pts
  • induction/aggr of abnormal blood lipid profiles
  • less sever w/ use of B1 blockers and B blockers w/ ISA (partial agonist activity)
41
Q

combination agent: nonselective B blocker and selective a1-blocker

A

Labetalol (Trandate)

42
Q

non-sel a blockers (a1&a2)

A

Phenoxybenzamine (Dibenzyline)

Phentolamine (gen. OraVerse)

43
Q

selective a1 blockers

A 
prazosin (minipress)
terazosin (hytrin)
doxazosin (cardura)
tamsulosin (flomax)
alfuzosin (uroxatral)
silodosin (rapaflo)
44
Q

a blocker mechanisms

A

-inhibition of vascular and other PERIPHERAL a-adrenergic recmost important

45
Q

B blockers are rev. competitive inhibitors and most a blockers are as well except

A

phenoxybenzamine: non comp. inhibition: TOXIC, irreversible, long acting
only syn. of new rec. can restore a adr. function

46
Q

a blockers inhibit

A

competitively, rel. fast, reversibly

47
Q

a1 blockers dec. BP primarily by dec..

A

peripheral vasc. resistance dued to inhibition of a1-med. arterial vasoconstriction

48
Q

common a-blocker side effects

A

-rel. to too much loss of a rec func.: nasal congestion, ejac. difficulties, reflex tachy, syst. EC fluid retention(over perfused capillaries), and othostatic hypotension

49
Q

Phenoxybenzamine

A

long-acting irrev. inhib of both a1 and a2 rec.

  • prev. sev. caechol. ind. HTN episodes occure in pheochromocytoma pt. during reop period prior to surgery, also to tx HTN in pts w/ pehochrom.
  • better than other a blockers bc irreversible,(others not going to overcome pheochrom.) (extrasyn. a2 more NE,E exposure)
50
Q

Phentolamin

A

rev. inhibs both a1, a2, short acting
dx. of pheochrom. “Phentolamine Test”
-during surge. rem of pheo.
-prev. rise in BP from cate. might be rel. from tumor DURING surgery
-to reverse acute syst. HTN from IV a agonist overdose (NE)
-prev. a agonist rel. local dermal tissue necrosis (NE spill)
-OraVerse (new) to rev. oral soft-tiss. anesthesia in dentistry
after vasoconstr. inj. (EPI)

51
Q

Prazosin

A

sel. a1 blocker
- long-term tx of mild-mod prim. HTN (esp. + diuretic)
- relax smooth musc. (sphincter) in bladder neck and prostatic urethra–>relieving obstructive urin. symps of BPH
- Raynaud’s syndrome (exc. response to cold stress)
- tx for nightmares rel. to PTSD (inh. of central a1 rec)

52
Q

Prazosin SEs

A

otho hypotension w. syncope (“first dose phenom”), Na/H2O retention (offset by diuretic), refl. tachy, (not as much w.non-sel: no inhib. of presyn. a2 med. neg fdbk control of NE rel from symp. nerve endings in SA node of heart) i.e. still get a2 med. neg fdback–>less NE rel. from SNS in SA node

53
Q

Doxazosin and Terazosin

A

newer a1 rec blockers
mechanism, SE and peripheral uses as prazoson longer 1/2 life better for chronic HTN and BPH, fewer doses (better compliance)
*not into CNS (can’t be used for PTSD)

54
Q

Tamsulosin and Silodosin

A

block subtype a1A receptors (subtype A) main type in sm. muscle of bladder nk and prostate vs. other a1 in BVs

  • tx BPH, more sp. w/ less syt. vasc actions and SEs (less dec. BP, syncope than other a1 blockers)
  • can still cause abn. ejaculation due to local inhib. of a1A rec in vas deferens
55
Q

Alfuzosin

A

block a1 rec for BPH but not rec subtype-sel, but shows “uroselectivity” for BPH but not sig. influencing vasc a1 rec (no BP, venous pooling effects)
-accumulation of alfuzosin in prostatic tissue (over 2x circulating plasma levels)

56
Q

Labetalol

A

combo nonsel B blocker and sel. a1 blocker
tx for mod-sev prim. HTN (oral) and emergency tx of HTN crisis (IV)
SE: bronchoconstriction, othostatic hypotention, less Raynaud’s (a blocked) and less reflex tachy (B blocked)

57
Q

sympathetic (adr) neuronal blockers: peripherally acting (inc. NE)

A

Reserpine*

Guanethidine

58
Q

centrally acting symp. neuronal blockers mechanism

A

stim. CNS a2 adr rec thus ind. reduce sympathetic neuronal traffic from central symp. vasomotor centers to peripheral CV organs

59
Q

centrally acting symp. neuronal blockers

A

methyldopa*
clonidine* (catapres)
guanfacine* (tenex, intuniv)
guanabenz (wytensin)

60
Q

Reserpine

A

dec. uptake of DA and NE into storage vesicle, deplete stored levels–>dec. amount rel–>reduced CO AND peri. art resistance–>reduces BP
Tx HTN
(will not get rebound)
(replaced by newer drugs, but less expensive)

61
Q

reserpine SE

A

sedation, mental depressiont (depl. action on CNS)
postural hypotension, brady, fluid retention (depleted peripheral sympathetics)
sev. diarrhea and ulcers (unopp. PSA)

62
Q

reserpine inactivation

A

unknown mech.

cleared fast, depletes NE irreversibly so long-acting

63
Q

Guanethidine

A

like reserpine: blocks uptake of DA and NE into storage vessels; but also DIRECTLY blocks NE release from nerve endings
-same peripheral BP effects as reserpine, not used to tx HTN in US anymore
must be taken up by reuptake pump of symp. NT, prevented by tricyclic antidepressants (imipramine, desipramine) these will interfere with/antagonize guanethidine effects

64
Q

Central acting adr. neuronal inhibitors

A

a2 rec agonist at various CNS sites: vasomotor centers in brain, red. symp. neuronal outflow–>dec to heart, vessels, kidney
-prevent rel. of NE (involves pre-syn. a2 rec)
-do not do much in periphery?? (mech of a2 rec) also conc. in CNS
tx for HTN
*do not interfere w/ normal reflex med. changes in symp nerve activity, fewer othostatic hypotensive symptoms, do not help for Raynaud’s
-little/no decrease in exercise capacity

65
Q

alpha-methyldopa

A

(prodrug, req. metab. to active form, some unique AI SEs)
DOPA–>DA–>NE enzymes also converted this prodrug to alpha-methylnorepinephrine–>a2 adr agonist in central vasomotor centers, dec. symp. outflow, art periph. resistance falls
–>dec. renal renin, dec HR, dec CO
tx: HTN second. to pregnancy
(no rebound HTN)

66
Q

alpha-methyldopa SE

A

fluid retention, dry-mouth, sedation (all a2 agonists)
induces “AI” disorders:
positive Coombs test: hemolytic anemia (easily rev.)
abnormal LFTs–>sev. necrosis

67
Q

Clonidine

A

direct a2 adr agonist, dec. symp outflow from CNS vasomotor centers
tx HTN
oral but dermal patch for smoother BP control, less SE except skin rxn
*SE: rebound HTN w/ abrupt cessation (like B blockers)

68
Q

other Clonidine uses

A

tx for w/drawal of addictive drugs (etOH, nicotine, morphine), ADHD, PTSD, hot flashes, migraine (rare)
-direct inj into spinal cord may have analgesic action: inhib rel of transmitters from terminals of aff. pain fibers (presyn. a2 agonist action in SC)

69
Q

apraclonidine (iopidine)

A
  • to lower postsurg IOP inc. by a2 agonist action in eye (brinonidine lowers IOP in glaucoma)
    (struct. rel to clonidine)
70
Q

Guanfacine

A

a2 anti HTN use (Tenex) like clonidine, but slightly less sedation and less tendency towards rebound
-ADHD tx (intuniv)

71
Q

Guanabenz

A

sim. to clonidine, tx for HTN

also: lowers tot. serum cholesterol, causes less reactive fluid retention (may not need diuretic)

72
Q

Nicotine

A

stimulant at low doses (nicotinic agonist) but depressant at v. high doses in all organs where ACh is NT and rec is nicotinic

stim: normal depot of cell men around mic rec
depress: persistent depol–>desensitation

73
Q

ganglionic stimulants

A

nicotine:

Nicorette, NicoDerm, Nicotrol

74
Q

ganglionic blockers

A

Mecamylamine (Inversine)

others: trimethaphan, hexamethonium

75
Q

sites of nicotine action

A 
CNS 
CV
GI
Skel muscels
*affects all nicotinic rec. subtypes, will stimulate/block(if high dose) dominant receptor
76
Q

CNS nicotine effects

A

-addiction tx
initially stimulation: inc. respiration
-can cause vomiting (CRTZ)
at higher doses, CNS stim–>depression

77
Q

CV nicotine effects

A

complex, at low dose: stim ANS–>adrenergic(symp) predom: inc. periph vasoconstriction w/ acute HTN
at higher doses: drop in BP

78
Q

GI nicotine effects

A

(ANS)

increase GI motility at low doses, opp. @ high doses

79
Q

nicotinic toxicity

A

as levels rise, symptoms may change to other types
tx largely symptom-directed; may need support of adrenergic agonists if NT blocked by high nicotinic levels
-if skel. musc blockade occurs, may need to support respiration
-

80
Q

nicotine absorption, excretion

A

rapid acting, absorbed from all routes
metab. in liver, excr. by kidney as cotinine
passes placental barrier and BBB

81
Q

nicotine therapy

A

smoking cessation (may inc. BP)
start high–>taper to wean off addiction
-warns against concurrent tobacco use

82
Q

risks of nicotine tx

A
  • accidental nicotine ingestion from E-cig (not FDA approved) refill solutions, insecticides, and tobacco products
  • field workers: dermal nicotine absorb from wet tobacco leaves: Green tobacco sickness
83
Q

Mecamylamine

A

ganglionic blocker, discontinued

tx: v. severe/malignant HTN (high doses), Tourette’s, suppress nicotine addiction (low doses)

84
Q

B1 blocker SE: removal of warning sign of tachycardia

A

going into hypoglycemia (for insulin-taking pts)

-pay attention to sweating! not affected by B-blockers

85
Q

B1 blocker SE: when suddenly removed

A

rebound HTN and/or angina

due to rec. up-regulation while blocking (potential for MI!)

86
Q

Labetalol tx

A

mod-sev. prim. HTN and emerg. tx of HTN crisis (IV)

-dec. art resist: a-block, partial B2 agonist, renin-reducing, dec. CO

87
Q

Labetalol SE

A 
orthostatic hypotension (a-block)
bronchoconstriction (B-block)
less Raynaud's (B-block) and tachy (a-block) seen with others
88
Q

phenoxybenzamine SE

A

inhib. some non-adr. rec (hist, ser, Ach)
miosis, sedation, drowsiness, vom, leth (CNS)
shock, circ. failure

89
Q

phentolamine SE

A

N/V/D
inc. GI motility (bad for ulcers)
may stim. or block non-adr. rec.

90
Q

mechanism of peripherally acting adr. neuronal inhibitors

A

dec. NE available to adr. rec of peripheral postgang SN endings

91
Q

guanethidine SE

A

postural hypotension, bradycardia, fluid retention
diarrhea, aggrav. of peptic ulcers, etc (like reserpine)
no CNS effects (unlike reserpine)

92
Q

Raynaud’s

A

abnormally exaggerated THERMAL reflex-mediated increase in SNA to blooc vessels in response to cold or emotional stress

93
Q

nicotine toxicity is usually not fatal bc

A

nicotine is inactivated quickly: 1/2 life of 2 hours

94
Q

mecamylamine: mechanism of gang. blockade

A

block neuronal nicotinic rec. (blocks pre–>post gang. transmission)

  • does NOT affect post-gang autonom. nerve terminals or rec. sites (can still respond to autonomic agonists like musc. and adr. rec stimulants)
  • does not affect muscular subtype nicotinic receptors (only neural) of NMJ in skel musc (can still move)
95
Q

mecamylamine adverse reactions

A

postural hypotension (interfere with compensatory baroreflexes)
dry mouth, diff swallowing
dec. GI, GU motility
mydriasis, cycloplegia (intol. to light, blurred vision)
sedation and other CNS side effects

96
Q

antidotes for too much gang. blockade

A

i.e. NE for CV support if neurogenic shock

97
Q

absorption, fate, excretion of mecamylamine

A

good GI absorb. (oral), crosses BBB and placenta, elimited mostly via renal excretion, 10 hr duration

Pharm (45 decks)

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