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NERB > Pharm Part 2 > Flashcards

Pharm Part 2 Flashcards

1
Q

Competitive muscarinic receptor blockers

A
  • atropine, scopolamine, propantheline, are sometimes used to control salivary secretions
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2
Q

Atropine

A
  • competitive muscarinic receptor blocker
    blocks vagal reflexive control of heart rate => results in tachycardia
  • don’t use anti-cholinergics in glaucoma pts bc it will increase their intra-occ pressure
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3
Q

Physostigmine

A
  • reversible anticholinesterase, - acts both centrally and peripherally, has some direct Ach like activity at neuromuscular junction, in addition to prolonging the activity of endogenous Ach
  • lipid-soluble drug that is absorbed very well orally
  • used to treat glacoma and Alzhmers
  • sometimes for treating xerostomia
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4
Q

Neostigmine

A
  • reversible anticholinesterase, - acts peripherally only, has some direct ACh-like activity at NMJ => prolongs activity of endogenous ACh, sometimes for treating xerostomia
  • also used for managing myasthenia gravis
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5
Q

Direct acting cholinergic agonists

A

pilocarpine, choline esters (drugs end in either choline or -ol for ester), may be used for xerostomia

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6
Q

Pralidoxime

A

enzyme regenerator used in organophosphate toxicity

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7
Q

Organophosphates and insecticides irreversibly inhibit

A

cholinesterase

- causing respiratory paralysis

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8
Q

Organophosphates

A

malathion and parathion

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9
Q

Synthetic versions of atropine

A

methantheline and propantheline both act only peripherial

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10
Q

what muscarinic receptor blockers can relieve some symptoms of Parkinson Disease

A

Atropine and scopolamine

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11
Q

what autonomic can be used to diagnose myathenia graves

A

Edrophonium

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12
Q

Succinylcholine

A
  • agonist at nicotinic receptors,
  • depolarizing NMJ blocker subject to rapid inactivation by plasma pseudocholinesterase,
  • used to prevent laryngospasm
    paralyzing dose causes muscle relaxation
  • used to relax muscles during surgery
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13
Q

d-tubocurarine

A
  • antagonist at nicotinic Rs
  • blocks the receptor site from ACh
  • non-depolarizing neuromuscular junction blocker
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14
Q

Cevimeline

A

cholinergic agonist to treat xerostomia and Sjogrens

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15
Q

Ganglionic blockers

A

mecamylamine and trimethaphan produce orthostatic hypotension

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16
Q

Signs of cholinergic crisis

A
  • bradycardia
  • larimation
  • salivation
  • voluntary muscle weakness
  • diarrhea
  • bronchoconstriction
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17
Q

What would you use to treat cholinergic crisis

A

atrophine

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18
Q

What are the symptoms of scopolamine overdose

A
  • disorientation
  • confusion
  • hallucinations
  • burning dry mouth
  • hypertherma
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19
Q

How would you treat scopolamine overdose

A

physostigmine

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20
Q

What does betulirum toxin prevent

A

release for Ach

- Botox

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21
Q

Signs of Cholinergic Stimulation effects

A
  • miosis (constriction of pupils)
  • decrease intraocular pressure
  • bradycardia
  • vasodilation
  • increase salivation
  • increase acid secretion
  • increase spasmodic activity of GI tract
  • increase urination
    -bronchoconstriction
  • lacrimation
  • sweating
  • muscle tremors
  • ataxia (loss of bodily movement
    ACRONYM: SLUD
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22
Q

Causes of Epinephrine injection

A

increase BP

1) myocardial stimulation
2) increase HR
3) vasoconstriction due to alpha receptor stimulation increase blood flow to muscle b/c beta2 receptor vasodilator

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23
Q

Ephedrine

A
  • causes release of stored norepinephrine and acts at receptor itself
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24
Q

Amphetamine

A
  • stimulates release of stored norepinephrine and stimulates alpha receptors in CNS
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25
Q

TCA antidepressant

A
  • norepinephrine and serotonin reuptake inhibition
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26
Q

MAO inhibitors

A
  • blocks enzymatic destruction of monoamines (EPI, NE, Dopamine, & Serotonin)
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27
Q

Alpha1 receptor stimulation

A

vasoconstriction, urinary retention, mydriasis

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28
Q

Alpha2 receptor stimulation

A

hypotention, reduces sympathetic outflow from CNS

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29
Q

Beta1 receptor stimulation

A
  • increased heart rate, increased force of contraction,
  • located in kidney, increase renin i.e. increase BP
    positive inotropic (modified force and speed) and chronotropic (HR) actions
  • mainly NE
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30
Q

Beta2 receptor stimulation

A

bronchodilation, vasodilation, dilation of skeletal muscle

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31
Q

Levodopa with Carbidopa

A
  • levodopa: is a dopamine precursor that can cross the blood brain barrier
  • carbidopa: is a dopa decarboxylase converter blocker
  • used to treat Parkinson’s
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32
Q

Phentolamine

A

nonselective alpha blocker, will cause vasodilation

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33
Q

Isopreterenol

A

beta2 receptor stimulator

34
Q

Methoxamine

A

vasoconstrictor that stimulates alpha 1 receptors

35
Q

Albuterol

A

beta2 agonist for bronchodilatory effects

36
Q

Physiological antagonism

A
  • two drugs produce opposite effects but don’t act on the same receptor
  • ex: epinephrine and histamine, epinephrine and nitroglycerin
37
Q

Idiosyncratic reactions

A
  • genetically determined abnormal responses to a drug, are most unpredictable because may not be shown until drug is taken for the first time by a pt
  • ex: succinylcholine and atypical plasma cholinesterase
38
Q

Benzodiazepines

A
  • modulates the action of inhibitory neurotransmitter GABA, many form active metabolites, is most common drug group given for oral sedation
  • ex: diazepam, chlordiazepoxide
39
Q

Benzodiazepines > barbiturates

A

less addiction potential, less profound CNS depression, larger therapeutic index, less respiratory depression

40
Q

Benzodiazepine adverse effects

A

IV injection of diazepam can cause irritation like thrombophletbitis due to solvent (propylene glycol)

41
Q

Diazepam

A

benzodiazepine, Valium, is given most commonly for oral sedation

42
Q

Triazolam

A

benzodiazepine, Halcion, is ultrashort acting version

43
Q

Midazolam

A

benzodiazepine, water soluble (doesn’t cause thrombophlebitis), shorter acting than valium because it doesn’t have active metabolites, has more rapid and predictable onset of action when given IM than valium

44
Q

Barbiturates

A

CNS depressants, will depress all levels of CNS, they are sedatives, not analgesic, will often induce excessive salivation and bronchial secretion and require use of anticholinergic drug to reduce these, are metabolized by the liver, are classified according to duration of action

45
Q

Thiopental

A

action is terminated by redistribution of drug out of the brain, will enter and exit the brain rapidly, thus quick onset and short duration of action

46
Q

Phenobarbital

A

long acting barbiturate

47
Q

Barbiturate toxicity

A

overdose kills you because of respiratory depression

48
Q

Barbiturate contraindications

A
  • intermittent porphyria: will enhance porphyrin synthesis and will aggravate the disease
  • undiagnosed severe pain: may make the pain worse and result in arousal, rage, delirium
    emphysema
49
Q

Barbiturate toxicity treatment

A

need to maintain open airway, increase input of afferent stimuli, maintain respiration, administer CNS stimulant

50
Q

1st generation antipsychotic drugs

A

Phenothiazine(Chlorpromazine) or Haloperidol, specific D2 (dopamine) receptor blocker

51
Q

Side effects of 1st generation antipsychotic drugs

A

anticholinergic effects and anti-a-adrenergic effects (xerostomia and postural hypotension), and extrapyramidal stimulation resulting in tardive dyskinesia, may have jaundice due to allergic reaction

52
Q

2nd generation antipsychotic drugs

A

Clozapine, block dopamine receptors and serotonin 5HT receptors, treat negative and positive symptoms, have fewer extrapyramidal side effects

53
Q

Antipsychotics

A

mostly dopaminergic receptor blockers in the brain

54
Q

Chlorpromazine

A

prototypic phenothiazine, used in treatment of schizophrenia

55
Q

Tricycline antidepressants

A

Imipramine or Amitriptyline, are reuptake inhibitors for amine neurotransmitters, were most commonly used in the past, are strong anticholinergics

56
Q

MAO inhibitors

A

Tranylcypromine or Phenylene

57
Q

SSRI antidepressant drugs

A

Fluoxetine/Prozac or Trazadone, much more commonly used now, block amine reuptake or alterations of receptor number

58
Q

Side effects of SSRI antidepressant drugs

A

anticholinergic side effects

59
Q

Lithium

A

drug of choice for manic phase of manic depression (bipolar disorder)

60
Q

Corticosteroids or glucocorticoids

A

suppress immune system in addition to anti-inflammatory activity, so latent infection like TB may go systemic and opportunistic infections like Candidiasis may become more of a problem

61
Q

Side effects of corticosteroids or glucocorticoids

A

gastric ulcers, immunosuppression, acute adrenal insufficiency (dec in cortisol & aldo), osteoporosis, hyperglycemia, redistribution of body fat

62
Q

General anesthesia onset and rate of induction

A

inversely proportional to solubility of anesthetic in the blood(more bl soluble, the more must be given to reach critical level), also influenced by pulmonary ventilation, blood supply to lungs, concentration of anesthetic in inspired mixture

63
Q

Halothane

A

associated with hepatotoxicity, may use atropine before to reduce salivation and bronchial secretions

64
Q

Stages of anesthesia

A

I: analgesia
II: delirium
III: surgical anesthesia
IV: medullary paralysis (once you start depressing medullary centers, pt will stop breathing and die)

65
Q

Moderate acting anesthetics

A

prilocaine, mepivacaine, lidocaine

66
Q

Long acting anesthetics

A

bupivacaine, tetracaine, etidocaine

67
Q

Lidocaines interaction with propranolol

A

interacts with propranolol by slowing down heart via beta receptor blockade and keeping lidocaine in the circulation longer and causing toxicity and by competing for the same enzyme in the liver

68
Q

Antibiotics interaction with coumarin

A

deplete vitK sources so will enhance coumarin anticoagulants

69
Q

Antibiotics interaction with oral conctraceptives

A

suppress normal flora involved in active steroids from bile conjugates => more rapid excretion of steroid from body

70
Q

Macrolide interactions

A
  • inhibit metabolism of drugs like seldane, digoxin
  • erythromycin blocks the metabolism of seldane to antihistamine metabolity => will stay unmetabolized and cause cardiac arrhythmias
71
Q

H1 antihistamines

A

Tx derm manifests of an allergy (cholpheniramine), pre-op med for sedation, aniemetic and anticholinergic effects (promethazine), control parkinsons sx (diphenhydramine)

72
Q

H2 antihistamines

A

Reduce gastric acid secretion (cimetidine)

73
Q

Promethazine

A

most common pre-op antihistamine med

74
Q

Diphenhydramine

A

used to control sx of parkinsons bc cholinergic and dopaminergic tracts interact in the brain, and thus anticholinergics will enhance dopaminergic fxns. antihis drugs have anticholinergic properties.

75
Q

what is the physiologic antagonist if histamine?

A

epi

76
Q

Drug used to tx trigeminal nueralgia?

A

carbamazepine and phenytoin

77
Q

Epi as a VC… main bad SE?

A

cardiac arrythmia

78
Q

how do sulfonyl ureas cause insulin secretion?

what effect to alpha and beta agonists, and cholinergics, have on insulin secretion?

A

direct stimulation of panc beta cells

alpha - dec insulin; beta - inc insulin; mAch - inc insulin

79
Q

Drug induced gingival hyperplasia

A
  • anticonvulsants (phenytoin, phenobarbital, lamotrigine, valproate, vigabatrin, ethosuximide, topiramate and primidone)
  • calcium channel blockers, such as nifedipine, amlodipine, and verapamil.
  • cyclosporine, an immunosuppresant
80
Q

Best drug to reverse the effects of benzodiazepines

A

Flumazenil

NERB (3 decks)

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