Pharm Part 2 Flashcards
Competitive muscarinic receptor blockers
- atropine, scopolamine, propantheline, are sometimes used to control salivary secretions
Atropine
- 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
Physostigmine
- 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
Neostigmine
- 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
Direct acting cholinergic agonists
pilocarpine, choline esters (drugs end in either choline or -ol for ester), may be used for xerostomia
Pralidoxime
enzyme regenerator used in organophosphate toxicity
Organophosphates and insecticides irreversibly inhibit
cholinesterase
- causing respiratory paralysis
Organophosphates
malathion and parathion
Synthetic versions of atropine
methantheline and propantheline both act only peripherial
what muscarinic receptor blockers can relieve some symptoms of Parkinson Disease
Atropine and scopolamine
what autonomic can be used to diagnose myathenia graves
Edrophonium
Succinylcholine
- 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
d-tubocurarine
- antagonist at nicotinic Rs
- blocks the receptor site from ACh
- non-depolarizing neuromuscular junction blocker
Cevimeline
cholinergic agonist to treat xerostomia and Sjogrens
Ganglionic blockers
mecamylamine and trimethaphan produce orthostatic hypotension
Signs of cholinergic crisis
- bradycardia
- larimation
- salivation
- voluntary muscle weakness
- diarrhea
- bronchoconstriction
What would you use to treat cholinergic crisis
atrophine
What are the symptoms of scopolamine overdose
- disorientation
- confusion
- hallucinations
- burning dry mouth
- hypertherma
How would you treat scopolamine overdose
physostigmine
What does betulirum toxin prevent
release for Ach
- Botox
Signs of Cholinergic Stimulation effects
- 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
Causes of Epinephrine injection
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
Ephedrine
- causes release of stored norepinephrine and acts at receptor itself
Amphetamine
- stimulates release of stored norepinephrine and stimulates alpha receptors in CNS
TCA antidepressant
- norepinephrine and serotonin reuptake inhibition
MAO inhibitors
- blocks enzymatic destruction of monoamines (EPI, NE, Dopamine, & Serotonin)
Alpha1 receptor stimulation
vasoconstriction, urinary retention, mydriasis
Alpha2 receptor stimulation
hypotention, reduces sympathetic outflow from CNS
Beta1 receptor stimulation
- 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
Beta2 receptor stimulation
bronchodilation, vasodilation, dilation of skeletal muscle
Levodopa with Carbidopa
- levodopa: is a dopamine precursor that can cross the blood brain barrier
- carbidopa: is a dopa decarboxylase converter blocker
- used to treat Parkinson’s
Phentolamine
nonselective alpha blocker, will cause vasodilation
Isopreterenol
beta2 receptor stimulator
Methoxamine
vasoconstrictor that stimulates alpha 1 receptors
Albuterol
beta2 agonist for bronchodilatory effects
Physiological antagonism
- two drugs produce opposite effects but don’t act on the same receptor
- ex: epinephrine and histamine, epinephrine and nitroglycerin
Idiosyncratic reactions
- 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
Benzodiazepines
- modulates the action of inhibitory neurotransmitter GABA, many form active metabolites, is most common drug group given for oral sedation
- ex: diazepam, chlordiazepoxide
Benzodiazepines > barbiturates
less addiction potential, less profound CNS depression, larger therapeutic index, less respiratory depression
Benzodiazepine adverse effects
IV injection of diazepam can cause irritation like thrombophletbitis due to solvent (propylene glycol)
Diazepam
benzodiazepine, Valium, is given most commonly for oral sedation
Triazolam
benzodiazepine, Halcion, is ultrashort acting version
Midazolam
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
Barbiturates
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
Thiopental
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
Phenobarbital
long acting barbiturate
Barbiturate toxicity
overdose kills you because of respiratory depression
Barbiturate contraindications
- 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
Barbiturate toxicity treatment
need to maintain open airway, increase input of afferent stimuli, maintain respiration, administer CNS stimulant
1st generation antipsychotic drugs
Phenothiazine(Chlorpromazine) or Haloperidol, specific D2 (dopamine) receptor blocker
Side effects of 1st generation antipsychotic drugs
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
2nd generation antipsychotic drugs
Clozapine, block dopamine receptors and serotonin 5HT receptors, treat negative and positive symptoms, have fewer extrapyramidal side effects
Antipsychotics
mostly dopaminergic receptor blockers in the brain
Chlorpromazine
prototypic phenothiazine, used in treatment of schizophrenia
Tricycline antidepressants
Imipramine or Amitriptyline, are reuptake inhibitors for amine neurotransmitters, were most commonly used in the past, are strong anticholinergics
MAO inhibitors
Tranylcypromine or Phenylene
SSRI antidepressant drugs
Fluoxetine/Prozac or Trazadone, much more commonly used now, block amine reuptake or alterations of receptor number
Side effects of SSRI antidepressant drugs
anticholinergic side effects
Lithium
drug of choice for manic phase of manic depression (bipolar disorder)
Corticosteroids or glucocorticoids
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
Side effects of corticosteroids or glucocorticoids
gastric ulcers, immunosuppression, acute adrenal insufficiency (dec in cortisol & aldo), osteoporosis, hyperglycemia, redistribution of body fat
General anesthesia onset and rate of induction
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
Halothane
associated with hepatotoxicity, may use atropine before to reduce salivation and bronchial secretions
Stages of anesthesia
I: analgesia
II: delirium
III: surgical anesthesia
IV: medullary paralysis (once you start depressing medullary centers, pt will stop breathing and die)
Moderate acting anesthetics
prilocaine, mepivacaine, lidocaine
Long acting anesthetics
bupivacaine, tetracaine, etidocaine
Lidocaines interaction with propranolol
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
Antibiotics interaction with coumarin
deplete vitK sources so will enhance coumarin anticoagulants
Antibiotics interaction with oral conctraceptives
suppress normal flora involved in active steroids from bile conjugates => more rapid excretion of steroid from body
Macrolide interactions
- inhibit metabolism of drugs like seldane, digoxin
- erythromycin blocks the metabolism of seldane to antihistamine metabolity => will stay unmetabolized and cause cardiac arrhythmias
H1 antihistamines
Tx derm manifests of an allergy (cholpheniramine), pre-op med for sedation, aniemetic and anticholinergic effects (promethazine), control parkinsons sx (diphenhydramine)
H2 antihistamines
Reduce gastric acid secretion (cimetidine)
Promethazine
most common pre-op antihistamine med
Diphenhydramine
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.
what is the physiologic antagonist if histamine?
epi
Drug used to tx trigeminal nueralgia?
carbamazepine and phenytoin
Epi as a VC… main bad SE?
cardiac arrythmia
how do sulfonyl ureas cause insulin secretion?
what effect to alpha and beta agonists, and cholinergics, have on insulin secretion?
direct stimulation of panc beta cells
alpha - dec insulin; beta - inc insulin; mAch - inc insulin
Drug induced gingival hyperplasia
- anticonvulsants (phenytoin, phenobarbital, lamotrigine, valproate, vigabatrin, ethosuximide, topiramate and primidone)
- calcium channel blockers, such as nifedipine, amlodipine, and verapamil.
- cyclosporine, an immunosuppresant
Best drug to reverse the effects of benzodiazepines
Flumazenil
