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PDA II > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

neurotransmitter that causes contraction of voluntary muscles

A

acetylcholine (ACh)

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2
Q

blood vessels only get ________ (sympathetic or parasympathetic) innervation

A

sympathetic

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3
Q

neurotransmitter released by preganglionic neuron in parasympathetic (cholinergic)

A

ACh

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4
Q

neurotransmitter released by postganglionic neuron in parasympathetic (cholinergic)

A

ACh

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5
Q

neurotransmitter released by preganglionic neuron in sympathetic (adrenergic)

A

ACh

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6
Q

neurotransmitter released by postganglionic neuron in sympathetic (adrenergic)

A

norepinephrine (NE)

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7
Q

only source of epinephrine is _______

A

adrenal medulla

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8
Q

synthesize and release ACh as the neurotransmitter, ALL preganglionic nerve fibers (parasympathetic/sympathetic), ALL parasympathetic postganglionic nerve fibers, FEW sympathetic postganglionic nerve fibers (sweat glands, because ACh is responsible for secretions)

A

cholinergic nerve fibers

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9
Q

synthesize and release NE as the neurotransmitter, NO preganglionic nerve fibers, ALL sympathetic postganglionic nerve fibers EXCEPT sweat glands

A

adrenergic nerve fibers

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10
Q

sympathetic effects on the eye (pupils, ciliary muscle/lens)

A

dilated pupils, far vision

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11
Q

parasympathetic effects on the eye (pupils, ciliary muscle/lens)

A

constricted pupils (miosis), near vision

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12
Q

sympathetic effects on the heart

A

increase HR and contractility

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13
Q

parasympathetic effects on the heart

A

decrease HR and contractility

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14
Q

sympathetic effects on the bronchi

A

dilated

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15
Q

parasympathetic effects on the bronchi

A

constricted

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16
Q

sympathetic effects on the GI system (motility and secretions)

A

inhibited

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17
Q

parasympathetic effects on the GI system (motility and secretions)

A

stimulated

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18
Q

sympathetic effects on the bladder

A

dilation (relaxation), urinary retention

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19
Q

parasympathetic effects on the bladder

A

constriction, urination

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20
Q

sympathetic effects on glucose release from the liver

A

stimulated

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21
Q

parasympathetic effects on glucose release from the liver

A

inhibited or no effect

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22
Q

synthesis of acetylcholine is inhibited by ________

A

hemicholinium

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23
Q

uptake of ACh into vesicles is inhibited by ________

A

vesamicol

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24
Q

release of ACh from the synapse is inhibited by _______

A

botox

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25
Q

binding of ACh to receptors is affected by _________

A

cholinergic receptor agonists and antagonists

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26
Q

degradation of ACh by AChE is inhibited by _________

A

AChE inhibitors

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27
Q

in plasma, ACh is degraded by _____________

A

butyrylcholinesterase (pseudocholinesterase)

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28
Q

why can’t we use ACh as a drug on its own?

A

it is quickly degraded in the plasma by cholinesterases

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29
Q

receptors that are activated by muscarine (alkaloid from Amanita muscaria), parasympathetic receptors on target tissues (CNS, cardiac muscle, smooth muscle, glands)

A

muscarinic receptors

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30
Q

receptors that are activated by nicotine (alkaloid from tobacco), Nn receptors (autonomic ganglia, adrenal medulla, CNS) and Nm receptors (receptors at neuromuscular junction/NMJ of skeletal muscle)

A

nicotinic receptors

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31
Q

which muscarinic receptors are coupled to Gq?

A

M1, M3, M5

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32
Q

which muscarinic receptors are coupled to Gi?

A

M2 and M4

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33
Q

which muscarinic receptors increase intracellular Ca2+ for contraction or secretion and are expressed in smooth muscles?

A

M1, M3, M5

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34
Q

which muscarinic receptors are expressed in the heart and decrease contractility/HR

A

M2, M4

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35
Q

what does DUMBBEELS stand for and what does it represent?

A

Diarrhea, Urination, Miosis, Bronchoconstriction, Bradycardia, Excitation, Emesis, Lacrimation, Salivation, Sweating
Muscarinic/Cholinergic effects

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36
Q

which receptors are ligand-gated ion channels and are fastest acting?

A

Nm, Nn

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37
Q

which receptors are coupled to Gq, are active in blood vessels, iris, sphincters, prostate, and activation causes smooth muscle contraction?

A

alpha 1

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38
Q

which receptors are coupled to Gi, are inhibitory autoreceptors on presynaptic sympathetic nerves (sensor), and activation inhibits NE release (negative feedback)

A

alpha 2

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39
Q

which receptors are coupled to Gs, expressed in cardiac monocytes, juxtaglomerular cells in kidney, increase heart rate and force of contraction, renin release in kidneys (increase blood pressure)

A

beta 1

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40
Q

which receptors are coupled to Gs, expressed in smooth muscles (bronchi, bladder, liver), bronchodilation, bladder relaxation, glycogenolysis and gluconeogenesis in liver to increase glucose levels

A

beta 2

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41
Q

nutritional supplements that act as anti-resorptive agents

A

calcium, calcium carbonate, calcium citrate, calcium phosphate, calcium lactate, calcium gluconate, vitamin D, ergocalciferol, cholecalciferol, calcitriol

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42
Q

commonly used due to the higher ratio of calcium to total weight - requires an acidic environment for absorption, to be taken with meals (which stimulates acid secretion) to improve absorption, drug interactions with proton pump inhibitors/H2 blockers/antacids because they decrease the absorption due to less stomach acid

A

calcium carbonate

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43
Q

less dependent on acid secretion for absorption compared to other calciums, useful in patients with achlorhydria (absence of HCl in stomach), inflammatory bowel disease, absorption disorders, or who are taking PPIs/H2 blockers, adverse effects include GI disturbances like constipation, kidney stones

A

calcium citrate

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44
Q

form of vitamin D from animal sources

A

cholecalciferol

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45
Q

form of vitamin D from plant sources

A

ergocalciferol

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46
Q

pharmacologically active form of vitamin D

A

calcitriol

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47
Q

supplementation with this in combination with calcium improves calcium absorption and improves bone mineral density which reduces the incidence of bone fractures, adverse effects include hypercalcemia, hypercalciuria, nephrolithiasis because the calcium can precipitate

A

vitamin D

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48
Q

in patients with severe hepatic or renal disease, which form of vitamin D should be administered because the other versions require hydroxylation by these organs?

A

calcitriol (pharmacologically active form)

49
Q
  • MOA: analogs of pyrophosphate - bind to calcium and get incorporated into bone matrix and taken up by osteoclasts, these drugs inhibit prenylation (attachment of certain lipids) to multiple proteins, decrease in osteoclastic activity, osteoclast apoptosis, increased bone density
  • very poorly absorbed orally and presence of food decreases oral bioavailability, must be given on empty stomach or IV
  • 50% of dose acculates in bones and remains for months, long biological half lives of up to 10 years which is the rationale for drug holidays
  • excreted unchanged in the urine (no liver metabolism)
  • mainstay agents to prevent and treat osteoporosis
A

bisphosphonates - alendronate, risedronate, ibandronate, zoledronate, pamidronate

50
Q

which bisphosphonate has greatest bone absorption and longest bone retention, given as IV infusion yearly or every two years?

A

zoledronate

51
Q

which bisphosphonates are administered on a daily, weekly, monthly basis?

A

alendronate, risedronate, ibandronate, pamidronate

52
Q

which bisphosphonates (oral or IV) have adverse effects of heartburn, dyspepsia, esophageal irritation and ulcer (recommend to take on empty stomach with glassful of water and remain upright for 30 mins after taking), and osteonecrosis of the jaw?

A

oral

53
Q

which bisphosphonates (oral or IV) have adverse effects of flu like symptoms, musculoskeletal pain, and osteonecrosis of the jaw?

A

IV

54
Q

natural ligand that acts on the receptors activator of nuclear factor kappa B present on osteoblast precursor cells and stimulates their differentiation into osteoclasts, bone resorption

A

RANK ligand (RANKL)

55
Q
  • MOA: inhibits binding of RANKL to RANK leading to decreased osteoclast formation and decreased bone resorption
  • used for postmenopausal osteoporosis, given SC every 6 months
  • adverse effect is hypocalcemia, FDA boxed warning that there is an increased risk for severe hypocalcemia for patients with advanced chronic kidney disease (CKD)
A

RANKL antagonist: denosumab

56
Q
  • drugs that bind to estrogen receptors and produce tissue-selective effects on target organs
  • MOA: inhibit osteoclast formation and recruitment, modestly increase bone density and decrease vertebral fractures (not as effective as estrogen)
  • advantage: reduces risk of breast cancer in postmenopausal women and in women with family history of breast cancer
  • for treatment and prevention of osteoporosis
  • adverse effects: hot flashes, venous thromboembolism
A

SERMs: raloxifene, bazedoxifene

57
Q
  • peptide hormone secreted by parafollicular cells of thyroid gland
  • function is to lower serum calcium levels by inhibiting bone resorption and calcium reabsorption in the kidney for more calcium excretion
  • MOA: inhibits osteoclastic bone resorption by converting active osteoclasts into resting stage, modest increase in bone mass
  • as an intranasal spray (preferred) or injection (SC, IM) for postmenopausal osteoporosis, not dosed orally because peptide, least effective as compared to other antiresorptive drugs
  • adverse effects: nasal form is rhinitis, epistaxis (nose bleeds), injection is nausea, flushing, irritation
A

calcitonin

58
Q
  • activate PTH1 receptors to increase osteoblast activity and number which increases bone mass and bone strength, increase in calcium absorption in GI tract and reabsorption in kidneys
  • reserved for patients with severe osteoporosis and glucocorticoid induced osteoporosis, approved for only 2 years of use, SC
  • adverse effects: orthostatic hypotension especially after first dose, dizziness, transient/temporary hypercalcemia
  • contraindications: patients at risk for osteosarcoma, patients with Paget disease, bone metastases/malignancies
A

PTH analogs: teriparatide, abaloparatide

59
Q
  • MOA: inhibits sclerostin (regulatory factor in bone metabolism), increases bone formation and to a lesser extent decreases bone resorption
  • for postmenopausal women with severe osteoporosis and patients who are intolerant or have failed other osteoporosis therapy, approved for only 1 year of use, given SC, anabolic effect wanes
  • adverse effects: arthralgia, headache, injection site pain, hypocalcemia (as calcium moves from blood to bone)
  • FDA boxed warning: risk of stroke, heart attack, death from cardiovascular problems
A

anabolic and antiresorptive agent: romosozumab

60
Q
  • MOA: bind directly with cholinergic receptors on effector organs and produces a parasympathetic effect
  • act at effector organs of postganglionic parasympathetic NS (M1-M5), autonomic ganglia (sympathetic and parasympathetic, Nn), certain brain synapses (CNS, Nn and M1), neuromuscular junction (NMJ, Nm)
A

direct acting cholinergic agonists

61
Q

esters of acetylcholine/analogs of ACh, nonselective against that act on both muscarinic and nicotinic receptors, quaternary amines with poor lipid solubility that don’t cross BBB so no central effects

A

direct acting cholinergic agents, choline esters: acetylcholine, bethanechol, carbachol

62
Q
  • resist hydrolysis so they are long-acting
  • muscarinic analogs so muscarinic selective (can’t act on nicotinic)
  • __________ is natural and acts on M1, 2, 3 receptors
  • __________ is synthetic and acts only on M1 and 3 so less cardiac side effects due to less binding on M2
  • tertiary amines with good lipid solubility that cross BBB so has central effects
A

direct acting cholinergic agents, alkaloids: pilocarpine, cevimeline

63
Q
  • MOA: inhibit AChE enzyme for less ACh degradation
  • activation of both muscarinic and nicotinic receptors in ANS, CNS, NMJ
  • decreased ACh degradation leads to increased ACh in synaptic cleft, increased ACh binding with receptors for parasympathetic effects
A

indirect acting cholinergic agents (acetylcholinesterase inhibitors)

64
Q

indirect acting cholinergic agents that are reversible inhibitors, carbamyl group is slowly removed from AChE, reversible inhibition of AChE since carbamylated AChE can’t breakdown ACh,

A

carbamates: neostigmine, physostigmine, pyridostigmine, rivastigmine, donepezil

65
Q

indirect acting cholinergic agents that are irreversible inhibitors, phosphate group is very slowly removed from AChE, irreversible inhibition leads to cholinergic toxicity seen with pesticide poisoning or nerve gases

A

organophosphates: echothiophate, malathion/parathion (pesticides), soman/sarin (nerve gases)

66
Q

heart rate decreases, contractile strength decreases, conduction velocity decreases, all via M2 receptors

A

effects of cholinergic agonists on heart

67
Q

stimulate M3 receptors on endothelial cells to produce nitric oxide which is a vasodilator and relaxes vascular smooth muscle cells leading to less resistance to blood flow for a decrease in blood pressure, all via M3 receptors

A

effects of cholinergic agonists on blood vessels

68
Q

contraction of bronchial smooth muscle or bronchoconstriction, increase resistance to airflow (asthma like state), increased mucus secretion from epithelial cells lining the airways, bronchorrhea (increased bronchial secretion), all via M3 receptors

A

effects of cholinergic agonists on respiratory system

69
Q

contraction of circular muscle for constriction of pupil (miosis), contraction of ciliary muscle for adaptation of lens for near vision, lacrimation (tears), increased aqueous humor outflow for decreased intraocular pressure (useful in glaucoma)

A

effects of cholinergic agonists on eyes

70
Q

stimulation of salivary glands and gastric gland secretions, increased motility of the GI tract/increased peristalsis, relaxation of sphincter muscles, promotes food digestion and defecation

A

effects of cholinergic agonists on GI system

71
Q

contraction of detrusor muscle (body of bladder), relaxation of internal sphincter muscles of the bladder, promotes urination

A

effects of cholinergic agonists on urinary system

72
Q

drugs used to treat open angle glaucoma

A

direct acting agonists (carbachol and pilocarpine), indirect acting agents (physostigmine and echothiophate)

73
Q

drugs used to treat xerostomia (dry mouth)

A

direct acting agonists (alkaloids - pilocarpine and cevimeline)

74
Q

drugs used to treat GI and urinary disorders

A

bethanechol to stimulate urination, neostigmine and pyridostigmine

75
Q

drugs used to treat myasthenia gravis, increase ACh levels selectively in NMJ because don’t cross BBB

A

neostigmine, pyridostigmine (longer acting)

76
Q

drugs to treat alzheimer’s disease, high lipid solubility to cross BBB (increase ACh selectively in CNS)

A

rivastigmine, donepezil

77
Q

what class of drugs are these (atropine, dicyclomine, scopolamine, homatropine, cyclopentolate, tropicamide, benztropine, trihexyphenidyl, oxybutynin, solifenacin, tolterodine)?

A

tertiary amines that cross BBB for central effects, anti-muscarinic/cholinergic

78
Q

what class of drugs are these (ipratropium, tiotropium, umeclidinium)?

A

quaternary amines that do not cross BBB for no central effects (charged at physiological pH), anti-muscarinic/cholinergic

79
Q

act as competitive antagonists - prevent ACh from binding to muscarinic receptors, effects can be overcome by increasing the concentration of muscarinic agonists which is useful when treating antimuscarinic toxicity/overdose

A

antimuscarinic MOA

80
Q

increased heart rate (tachycardia) and increased contractile strength via M2 blockade, minimal effects on blood vessels via M3 blockade (increased HR and cardiac output but no major change in blood pressure), used to treat sinus bradycardia (atropine)

A

antimuscarinic drugs on cardiovascular system

81
Q

bronchodilation via M3 receptor blockade (more pronounced in COPD, some in asthma), decreased mucus secretions via M3 blockade for drier airways which can counteract the stimulation of mucus secretion by anesthetics in surgery (preanesthetic medication to prevent mucus secretion, atropine), (ipratropium short acting, tiotropium/umeclidinium long acting for bronchodilators as inhalation)

A

antimuscarinic drugs on respiratory system

82
Q

prevents contraction of circular muscle which facilitates contraction of radial muscle for dilation (mydriasis) of the pupil, prevents contraction of the ciliary muscle for inability to adapt lens for near vision (cycloplegia), reduced lacrimation/tears leading to dry eyes, (homatropine, tropicamide, cyclopentolate for retina exams to dilate the pupils)

A

antimuscarinic drugs on eyes

83
Q

reduction of salivary secretion (dry mouth, common side effect), reduction of gastric acid secretion (but a large dose required), relaxation of GI smooth muscle (decreased motility/peristalsis and tone leading to constipation), clinical uses include atropine and diphenoxylate as an anti-diarrheal agent/IBS, and dicyclomine to slow bowel movement in IBS

A

antimuscarinic agents on GI

84
Q

relaxation of bladder muscle and ureter smooth muscle, contraction of bladder sphincter, urinary retention, oxybutynin, tolterodine, solifenacin, darifenacin, fesoterodine, trospium, to treat overactive bladder and nocturnal enuresis (bedwetting)

A

antimuscarinic drugs on genitourinary system

85
Q

centrally acting antimuscarinic drugs with high solubility to cross BBB to decrease ACh levels selectively in CNS, useful in this disease, benztropine, trihexyphenidyl, tertiary amines

A

parkinson’s disease

86
Q

what drug is used to treat anticholinergic toxicity because it is a tertiary amine that crosses BBB, inhibits ACh in the brain, increases ACh levels in the brain and displaces anticholinergic agent from muscarinic receptors, effects short lived leading to frequent dosing?

A

physostigmine

87
Q

drug used to treat respiratory muscle paralysis due to excessive activation of Nm receptors in NMJ and other symptoms in patients exposed to high doses of organophosphate insecticides or nerve gases, unable to cross BBB so atropine used in combo with this to treat both respiratory and CNS components of toxicity

A

pralidoxime (2-PAM)

88
Q

these receptors are coupled to Gq, found in smooth muscles and net effect is contraction

A

alpha 1

89
Q

these receptors are coupled to Gi, found in presynaptic nerve endings and net effect is inhibition of NE release

A

alpha 2

90
Q

these receptors are found in the heart and juxtaglomerular cells, coupled to Gs, net effect is increased HR/contractility, renin release

A

beta 1

91
Q

these receptors are found in the smooth muscle (bladder, bronchi) and liver, coupled to Gs, and net effect is bronchodilation, relaxation, glycogenolysis and gluconeogenesis

A

beta 2

92
Q

these adrenergic agonists bind to one or more subtypes of adrenergic receptors, can be selective or non-selective

A

direct acting

93
Q

these adrenergic agonists increase the availability of NE/Epi by releasing or displacing NE from nerve terminals (Amphetamine), blocking reuptake of NE (cocaine, atomoxetine, methylphenidate), inhibition of metabolizing enzymes (MAO - selegiline, COMT - entacapone)

A

indirect acting

94
Q

mediated via B1 receptors, increase in intracellular Ca2+ levels, increase contractile strength, increase HR, increase conduction velocity

A

adrenergic agonists on heart

95
Q

regulated mostly by a1 and some B2 receptors, a1 receptors located on arterial and venous smooth muscle, NE and a1 agonists (vasoconstriction and increased BP), B2 agonists (vasodilation and decreased BP, NE cannot act at B2 receptors so no significant vasodilation)

A

adrenergic agonists on blood vessels

96
Q

what drug is used to treat cardiogenic shock and heart failure due to inadequate perfusion of the tissues (increases HR and contractility by stimulating B1 receptors in the heart)?

A

dobutamine

97
Q

what drug is used to treat hypotension (increases BP by stimulating a1 receptors in blood vessels)?

A

phenylephrine

98
Q

what drug is used topically to reduce bleeding in surgical field during facial, oral, nasal surgery?

A

epinephrine

99
Q

what drugs are used to treat essential hypertension (no identifiable cause), a2 agonists stimulate presynaptic a2 receptors and reduce NE release from nerve terminals?

A

clonidine, methyldopa

100
Q

which drugs are used as topical decongestants in the upper respiratory system?

A

phenylephrine, oxymetazoline, tetrahydrozoline

101
Q

B2 agonists that are used as bronchodilators for asthma

A

albuterol, salmeterol, formoterol

102
Q

adrenergic agonists used to treat ophthalmic hyperemia (red eyes)

A

phenylephrine, oxymetazoline, tetrahydrozoline

103
Q

B3 receptor agonist that relaxes bladder detrusor muscle, used in treating overactive bladder

A

mirabegron

104
Q

NE releasing agents used in ADHD and narcolepsy

A

amphetamine, lisdexamfetamine

105
Q

NE reuptake inhibitor used in ADHD and narcolepsy

A

atomoxetine

106
Q

NE and DA reuptake inhibitor used in ADHD and narcolepsy

A

methylphenidate

107
Q

MAO inhibitor used in depression and parkinson’s disease

A

selegiline

108
Q

COMT inhibitor used in parkinson’s disease

A

entacapone

109
Q

selective a1 blockers used in BPH and HTN

A

prazosin (HTN), terazosin (HTN, BPH), doxazosin (HTN, BPH), alfuzosin (HTN, BPH), tamsulosin (BPH), silodosin (BPH)

110
Q

act as competitive antagonists at beta adrenergic receptors, antihypertensive effects through decreased HR/contractility and decreased renin release, mask hypoglycemia symptoms, contraindicated in sinus bradycardia, heart failure, partial AV block

A

beta blockers (-olols)

111
Q

which beta blockers are partial agonists?

A

pindolol and acebutolol

112
Q

which beta blockers are non-selective?

A

propranolol, nadolol, timolol, pindolol

113
Q

which beta blockers are beta 1 selective?

A

atenolol, metoprolol, esmolol, acebutolol

114
Q

bronchoconstriction and hypoglycemia happens with these beta blockers and are contraindicated in asthma and COPD

A

non-selective (beta 1 and 2)

115
Q

this beta blocker is used topically to treat glaucoma

A

timolol

116
Q

this beta blocker is used IV to treat intraoperative HTN and acute arrhythmias

A

esmolol

117
Q

this beta blocker is nonselective but also has alpha 1 selective activity

A

labetalol

118
Q

sudden withdrawal of this class of drugs causes rebound hypertension, arrhythmias, angina due to upregulation of beta 1 receptors during blockade, should not be withdrawn suddenly, should be tapered gradually

A

beta blockers

PDA II (4 decks)

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