Explain Pharmacokinetics - ANSWER-The study of how drugs are moved through the body and are encompassed in mechanisms
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Absorption
Distribution
Metabolism
Excretion
Think Kinetic (movement)
Pharmacodynamics - ANSWER-study of the biochemical and physiologic effects of drugs on the body
Think Dynamic (change)
majority of drugs either
(a) mimic or inhibit normal physiological/biochemical processes or inhibit pathological processes in animals or
(b) inhibit vital processes of endo- or ectoparasites and microbial organisms
Summarize the main drug actions - ANSWER-1 - stimulating action through direct receptor agonism and downstream effects
2 - depressing action through direct receptor agonism and downstream effects (ex.: inverse agonist)
3- blocking/antagonizing action (as with silent antagonists), the drug binds the receptor but does not activate it
4- stabilizing action, the drug seems to act neither as a stimulant or as a depressant
5- exchanging/replacing substances or accumulating them to form a reserve (ex.: glycogen storage)
Desired activity is achieved through what main mechanisms? - ANSWER--Cellular membrane disruption
-Chemical reaction with downstream effects
-Interaction with enzyme proteins
-Interaction with structural proteins
-Interaction with carrier proteins
-Interaction with ion channels
-Ligand binding to receptors: 1)Hormone receptors 2) Neuromodulator receptors 3)Neurotransmitter receptors
Explain the therapeutic window - ANSWER-therapeutic window is the amount of a medication between the amount that gives an effect (effective dose) and the amount that gives more adverse effects than desired effects
Duration of action - ANSWER-duration of action of a drug is the length of time that particular drug is effective
Explain bioavailability - ANSWER-drug's bioavailability can be defined as the proportion of the drug that reaches its site of action
6 rights to medication administration - ANSWER-RIGHT CLIENT
RIGHT MEDICATION
RIGHT DOSAGE
RIGHT ROUTE
RIGHT TIME
RIGHT DOCUMENTATION
Potency - ANSWER-potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity
(more morphine is needed to give the same effects as fentanyl)
Efficacy - ANSWER-Efficacy is the relationship between receptor occupancy and the ability to initiate a response at the molecular, cellular, tissue or system level. In other words, efficacy refers to how well an action is took after the drug is bound to a receptor
Affinity - ANSWER-Affinity is how well a drug can bind to a receptor (Fast/strong binding = higher affinity)
Benzodiazepine MOA - ANSWER-Act on GABA which is a major inhibitory NTM in the CNS; Effects are produced by interacting with a protein complex with in the neuronal membrane GABA which has a high 'affinity' for benzo's specifically;
Inhibition of polysynaptic afferent pathways resulting in skeletal muscle relaxation; It decreases the spread of seizure activity due to an increased pre-synaptic inhibition of the CNS
Benzodiazepine uses/indications - ANSWER-Similar actions however different doses/concentrations/combinations produce different actions thus have different uses
Anxiety/panic disorders
skeletal muscle relaxation
seizures
sedation for procedures (due to relaxation and amnesic properties)
Benzodiazepines adverse effects - ANSWER-Most derived through CNS actions; Ataxia, dizziness, drowsiness/sedation, blurred vision, hypnosis, weakness, fatigue
More severe: hypersensitivity, mental depression, hypotension, paradoxical stimulation, rebound seizures
Benzo pharmacokinetics - ANSWER-Widely distributed throughout the body
accumulate in lipid rich areas (CNS and adipose tissue)
the more lipophilic the agent the faster it is absorbed
Onset 30 min- 1 hr lasting 4-6 hours, peak at 1-2 hours
IV Admin: onset 1-5 min, peak immediately, last 15-20 min
metabolized by the liver and excreted in urine
Beta blocker (BB) MOA - ANSWER-Interrupts the nerve impulses across the neurons by antagonizing the receptors with in the cardiac cells resulting in blockade of the beta 1 receptors';
-B1 blockade results in reduction of heart rate (chronotropic), rate of conduction through the AV node (dromotropic), and force of contraction (inotropic)
This in turn decreases the oxygen demand on the myocytes, reduction in BP from the reduced HR and inotropic actions
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the hormone glucagon, which work together to increase plasma glucose
Beta blocker Therapeutic uses - ANSWER-Useful in angina, HTN, cardiac dysrhythmias, MI, HF, Hyperthyroidism, migraines, pheochromocytoma, Glaucoma
In angina/MI: reduction of oxygen demand
HTN: B1 blockade as well as suppressed renin release via B1 blockade in the kidneys shows a marked decrease in PVR which results in improved stroke volume
Beta Blocker Adverse effects - ANSWER-B1 blockade: bradycardia resulting in reduced CO and precipitating HF, AV heart block, Rebound cardiac Excitability
B2 effects incl: bronchoconstriction, and Inhibition of glycogenolysis resulting in hypoglycemia
Beta blocker Pharacokinetics - ANSWER-Highly lipid soluble
Absorption usually rapid/complete
50% 1st pass metabolism
peak concentrations approx. 1.5-2 hours, onset about 4-5 hrs
liver metabolized, renal excretion as a metabolite
Beta blocker interactions - ANSWER-Calcium channel blockers: Negative Ino/dromo/chronotropic effects
anti-arrhythmics: may enhance their effects leading to unwated outcomes
Nitrates: may potentiate hypotensive effects
MAO inhibitors: may increase reduction of sympathetic activity thus the inability to respond to Fight/flight mechanism resulting in reduced BP/HR overall
Digitalis: Can potentiate suppressed AV conduction
Calcium Channel Blockers (CCB) MOA - ANSWER-inhibition of calcium movement in smooth and cardiac muscle tissue by selectively antagonizing calcium influx movment across the cellular membrane responsible for smooth/cardiac muscle conduction velocity: produces relaxation of coronary smooth muscles, dilation of coronary arteries; reduced dromotropic effects of the sa/av node and reduced automaticity
Effects peripherally result in vasodilation through smooth muscle relaxation
Different agents have different effects on different receptors within the transmembrane calcium channels
Non specific effects in blood coagulation by inhibiting platelet aggregation in the clotting cascade
CCB indications - ANSWER-Hypertension, angina, dysrhythmias
CCB Adverse effects - ANSWER-Peripheral edema, flushing, palpitations, headache
Pulmonary edema, rebound tachycardia, bradycardia, skin rash
CCB drug interactions - ANSWER-BB and other antiarrhythmics can potentiate their effects
increased concentrations of theophyliine and digoxin may occur
Non-depolarizing Neuromuscular Blocker MOA - ANSWER-Prevent Ach from activating Nicotinic 'm' receptors on skeletal muscle, causing relaxation and flaccidity (does not cause depolarization at the neuromuscular endplate)
Competes with Ach for biding with Nm receptors, blocking Ach thus preventing stimulation causing the muscle to no longer be engaged and relax; effect lasts until there is insufficient amount available to overtake the Ach
(muscles paralyze at different times: Levator muscles of the eyelids first, than limbs, abdomen, and lastly the glottis diaphragm and intercostal)
Non-depolarizing Neuromuscular Blocker indications - ANSWER-To facilitate muscular relaxation for general procedures requiring its purose such as to facilitate ETI, Mechanical ventilation, Surgery
Non-depolarizing Neuromuscular Blocker Adverse effects - ANSWER-Hypotension: is due to release of histamine from mast cells and partial blockade of Nn receptors in the ANS by suppressing sympathetic tone to peripheral vasculature
Myasthenia gravis: condition characterized by an overall decreased number of Nm receptors thus a Nm blocking agent given in this subset could produce a more profound, rapid, and prolonged effect
Non-depolarizing Neuromuscular blocking agent drug interactions - ANSWER-Hypokalemia can enhance effects
Hyperkalemia can reduce effects
Aminoglycoside antibiotics (gentamycin, vancamyacin), tetracycline, non PCN antibiotics: can intensive the response to Nm blockade
Cholinesterase inhibitors: Decrease the effectiveness effectively reversing the Nm blockade due to an increased degredation of Ach @ the neuromuscular junction
Acetylcysteine (mucomyst, pravolex)
Mucolytic: MOA - ANSWER-Antidote to Acetaminophen: Exact mechanism is unknown however thought to restore hepatic glutathione and thus inactivating the toxic metabolite of acetaminophen, preventing further hepatic damage
Metabolite produced by acetaminophen: N-acetyl-p-benzoquinone imine (NAPQI) accumulates within the body. It is normally conjugated by glutathione, but when taken in excess, the body's glutathione reserves are not sufficient to inactivate the toxic NAPQI. This metabolite is then free to react with key hepatic enzymes, thereby damaging liver cells
Acetylcysteine (mucomyst, pravolex)
Mucolytic: MOA mucolytic - ANSWER-acts by splitting the bonds of mucoprotein (substance responsible for increased viscosity of mucous secretions in the lungs)
Acetylcysteine (mucomyst, pravolex)
Mucolytic: Indications - ANSWER-Acetaminophen Toxicity
Mucolytic action in acute and chronic bronchopulmonary disease; Tracheostomy care
Acetylcysteine (mucomyst, pravolex)
Mucolytic: Dose - ANSWER-Acetaminophen Toxicity:
150 mg/kg IV over 15 min
Repeated at 50mg/kg over 4 hours
Acetylcysteine (mucomyst, pravolex)
Mucolytic: Contraindications - ANSWER-HSN to drug
Status asthmaticus as it may precipitate bronchospasm
Activated Charcoal w sorbitol: MOA - ANSWER-Absorbs ingested toxins by inhibiting their absorption in the GI tract
Sorbitol is a sweetener and works as a laxative for the elimination of the poison from the body
Activated Charcoal w sorbitol: Dose - ANSWER-30-100 g in 250 ml water (5-10 times the estimated weight of the drug/chemical) PO/NG/OG
peds: 1-12 yo: 1 gm/kg
Activated Charcoal w sorbitol: Contraindications - ANSWER-Pt who has ingested corrosive agent or petroleum distillate
violent pt with ALOC
Altered pt and not intubated with no NG/OG in place
Activated Charcoal w sorbitol: Caution - ANSWER-Not effective for cyanide, mineral acids, caustic alkaloids, organic solvents, iron, ethanol, methanol, lithium
Can cause vomiting and can cause severe ALI if aspirated
Adenosine (adenocard)
antiarrhythmic (naturally occurring nucleoside): MOA - ANSWER-In the heart it acts on the AV node to slow conduction and inhibit reentry pathways
mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing K+ efflux via inward rectifier K+ channels, subsequently inhibiting Ca2+ current
Also produced coronary vasodilation
Adenosine (adenocard)
antiarrhythmic (naturally occurring nucleoside): Indications - ANSWER-Stable/unstable Narrow complex regular tachycardias
Adenosine (adenocard)
antiarrhythmic (naturally occurring nucleoside): Dose - ANSWER-(acls)
6 mg RAPID IVP (over 1-2s) followed by a rapid 20 ml NS bolus
Repeat x 2 at 12 mg RAPID IVP in 1-2 min (if no conversion)
Peds: 0.1 mg/kg Rapid IVP to a max of 6 mg
repeated at 0.2 mg/kg Rapid IVP max of 12 mg
Adenosine (adenocard)
antiarrhythmic (naturally occurring nucleoside): Contraindications - ANSWER-HSN to drug or any component
2/3rd degree block without a pacemaker
Sick sinus syndrome
Pre-excitation syndromes (AF/Aflutter/VT with accessory pathway like wpw as this may cause hemodynamically unstable ventricular response)
Adenosine (adenocard)
antiarrhythmic (naturally occurring nucleoside): Caution - ANSWER-caution in asthmatics as it can cause bronchoconstriction
caution in those taking carbamazepine (tegretol) or dipyrimdamole (persantine) as it may increase risk of progressive high heart blocks
pts who are on stimulants (caffeine) or theophylline may require larger doses as these drugs counter the effects of adenosine
Amiodarone HCL (codarone)
class III vw anti-arrhythmic: MOA - ANSWER-Amiodarone slows conduction rate and prolongs the refractory period of the SA and AV nodes
- and prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability. It has numerous other effects, however, including actions that are similar to those of antiarrhythmic classes Ia, II, and IV.
It also inhibits adrenergic stimulation and decreases peripheral vascular resistance- causing some vasodilation
Amiodarone HCL (codarone)
class III vw anti-arrhythmic: Indications - ANSWER-VF/Pulseless VT unresponsive to CPR and shock therapy
Hemodynamically stable monomorphic VT
Polymorphic VT with a normal QT interval
Stable irregular narrow complex tachycardia (AF < 48 hrs)
Stable regular Narrow complex tachycardia (unresponsive to adenosine/instances where adenosine is contraindicated)
Amiodarone HCL (codarone)
class III vw anti-arrhythmic: Dose - ANSWER-Cardiac arrest: 300 mg IVP diluted in 20 ml NS/D5W; repeated at 150 mg in 3-5 min
Recurrent life threating ventricular arrhythmias
Rapid Infusion: 150 mg/10 min (15 mg/min) q 10 min prn
Slow infusion: 360 mg IV over 6 hrs (1 mg/min)
Peds: VF/VT pulseless: 5 mg/kg IVP max of 300 mg, repeat twice
Ventricular tachyarrhythmias: 5 mg/kg IV over 20-60 min repeated prn max of 15 mg/kg or 2.2 g
Amiodarone HCL (codarone)
class III vw anti-arrhythmic: Contraindications - ANSWER-Av block, 2/3rd degree without a pacemaker
Bradycardia resulting in syncope as it may cause atropine resistant bradycardia
Sinus node impairment
Cardiogenic shock
sensitivity to amiodarone or iodine
thyroid disease
Other drugs that cause a prolonged QT (procainamide)
and stop infusion if QT widens by 50% of baseline or if hypotension results
Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen)
Salicylate, antiplatelet, antipyretic, anti-inflammatory: MOA - ANSWER-Anti-platelet: at low doses impedes clotting by inhibiting enzyme CoX-1 and prostaglandin synthesis which prevents formation of platelet aggregating substance Thromboxone A2 (this is irreversible and can prolong bleeding time)
All mechanisms are related to inhibition of CoX-1 and prostaglandin acting non specifically on the hypothalamus/platelets/ sites of injury
Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen)
Salicylate, antiplatelet, antipyretic, anti-inflammatory: Indications - ANSWER-Acute coronary syndromes
Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen)
Salicylate, antiplatelet, antipyretic, anti-inflammatory: Dose - ANSWER-160-325 mg Po as soon as possible (even if pt states they have taken their own)
Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen)
Salicylate, antiplatelet, antipyretic, anti-inflammatory: contraindications - ANSWER-HSN to ASA or other NSAIDs
Active GI bleeding
Acetylsalicylic acid/ASA (aspirin, bufferin, Novasen)
Salicylate, antiplatelet, antipyretic, anti-inflammatory: Cautions - ANSWER-Active ulcer disease
ashmatics
Bleeding disorders
Impaired renal/hepatic functions
Never given to children/adolescents with viral infections as it may precipitate reye's syndrome
Atropine
Anticholinergic: MOA - ANSWER-Blocking the effects of acetylcholine (parasympathetic tone) on the SA and AV nodes thereby increasing the SA and AV conduction velocity resulting in increased HR
Blocks the actions of parasympathetic nervous system and glands via the Ach receptor blockade producing reduced secretions on bronchial, salivary, and sweat glands
Atropine
Anticholinergic: Indications - ANSWER--Temporizing measure while awaiting a TCP for pt with symptomatic bradycardia, conduction block, sinus arrest
-reversal of neuromuscular blockade prior to admin of anticholinesterases (neostigmine) to -counter their cholinergic effects
-Organophosphate poisoning
-MFI with Ketamine: decreasing bronchial secretions due to the cholinergic effects of ketamine
Atropine
Anticholinergic: Dose - ANSWER-Symptomatic Bradycardia: 0.5 mg q 3-5 min prn max of 3 mg total
MFI w/ ketamine: 0.01 mg/kg IVP to 0.5 mg once
Organophosphate poisioning: 2 mg IVP q 5 prn
Peds: 0.2 mg/kg IV max single dose 0.5 mg
max total dose 1.0 mg
OP poisoning: 0.05 mg/kg IVP prn q 5 min
*** Note: smaller doses may precipitate paradoxical bradycardia (<0.5mg adult, <0.1mg ped)***
Atropine
Anticholinergic: contraindications - ANSWER-HSN
Glaucoma
Tachycardia
Atropine
Anticholinergic: Notes - ANSWER-Do not delay external pacing in pt with signs of poor perfusion
S/S of atropine (anti-cholinergic) overdose:
midriasis
agitation
dry skin
fever
flushed
(blind as a bat, mad as a hatter, dry as a bone, hot as a hare, red as a beet respectively)
Tx requires neostigmine
CaCl (calcium chloride)
Electolyte: MOA - ANSWER-Needed for maintenance of nervous, muscular, skeletal systems and enzyme reactions and normal cardiac contractility as well as blood coagulation
Affects secretory activity of the endocrine and exocrine glands
Is used as a membrane stabilizing measure in the presence of life threatening hyperkalemia
CaCl (calcium chloride)
Electolyte: Indications - ANSWER-Hyperkalemia
CCB overdose/BB overdose
Hypocalcemia
Hypermagnesemia
CaCl (calcium chloride)
Electolyte: Dose - ANSWER-500 - 1000 mg of 10% solution VERY SIVP (no more than 100 mg/min) prn
Peds: 20 mg/kg over 10 min prn
CaCl (calcium chloride)
Electolyte: Contraindications - ANSWER-Hypercalcemia
digitalis toxicity
renal calculi
VF (accept in the setting of suspected hyperkalemia)
CaCl (calcium chloride)
Electolyte: Cautions/notes - ANSWER-Monitor ECG/BP
Give slowly and stop if pt c/o discomfort
Avoid extravasiation as it can cause necrosis and sloughing of skin (administer in a large bore catheter)
Do not administer with NaHCO3 (bicarb) as it will form a precipitate
Clopidogrel (Plavix)
Platelet aggregation inhibitor: MOA - ANSWER-Inhibits binding of the adenoise Diphosphate (ADP) to its platelet receptor and the subsequent ADP mediated activation of glycoprotein IIb/IIIa complex, thus inhibiting platelet aggregation
Clopidogrel (Plavix)
Platelet aggregation inhibitor: Indications - ANSWER-STEMI
CVA
Clopidogrel (Plavix)
Platelet aggregation inhibitor: Dose - ANSWER-75 mg PO once daily
Clopidogrel (Plavix)
Platelet aggregation inhibitor: Contraindications - ANSWER-HSN
Active bleeding
Significant liver impairment or cholestatic jaundice (due to needing liver activation form is CYP pathway)
History of hepatitis/long term ETOH abuse/jaundiced
Thrombotic thrombocytopenia
Suspected aortic dissection
Acetaminophen (Tylenol, paracetamol)
Analgesic, Anti-pyretic: MOA - ANSWER-Acts on the hypothalamus to produce antipyresis
may work peripherally to pain impulse generation, via inhibition of prostaglandin synthesis in the CNS
Selective cyclooxygenase the enzyme needed to make prostalgandins and related compounds in the CNS (limited effects peripherally)
Prostaglandins are powerful locally acting vasodilators and inhibit the aggregation of blood platelets as well as found in almost EVERY tissue in the body. Through their role in vasodilation, prostaglandins are also involved in inflammation. They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the contraction of smooth muscle tissue, nervous system transmission etc.
Acetaminophen (Tylenol, paracetamol)
Analgesic, Anti-pyretic: Indications - ANSWER-Fever
Pain relief mild-moderate
Acetaminophen (Tylenol, paracetamol)
Analgesic, Anti-pyretic: Dose - ANSWER-Varies
typically 325- 1000 mg Po q 4 hr prn
Peds: 10-20 mg/kg q 6-8 hrs
Toxic dose is more than 150 mg/kg or 12 g of acetaminophen
Acetaminophen (Tylenol, paracetamol)
Analgesic, Anti-pyretic: - ANSWER-HSN
hepatitis/hepatic impairment, renal dysfunction/ severe alcoholism
history of hereditary angioedema
Acetaminophen (Tylenol, paracetamol)
Analgesic, Anti-pyretic: Adverse affects - ANSWER-Angioedema
disorientation
dizziness
rash
urticarial
GI bleeding
thrombocytopenia
nephrotoxicity
hepatotoxicity
Dexamethasone (decadron)
Glucocorticoid: MOA - ANSWER--Stimulates synthesis of enzymes needed to decrease inflammatory response
-reduces inflammation by suppressing the synthesis of inflammatory mediators, infiltration of phagocytes, release of lysosomal enzymes and proliferation of lymphocytes
-Crosses the placental barrier and promotes fetal lung maturation by increasing the production of surfactant
Dexamethasone (decadron)
Glucocorticoid: Indications - ANSWER-Anaphylaxis
bronchospasm
croup
Prevention of hyaline membrane disease in premature infants (24-34 wks)
Dexamethasone (decadron)
Glucocorticoid: Dose - ANSWER-varies
8-10 mg IV/IM/PO
premature delivery: 5 mg IVP/IMtid 24-48 hrs prior to delivery
Peds: 0.6 mg/kg (typically 2-4 mg) IV/IM/PO max of 16 mg/day
Dexamethasone (decadron)
Glucocorticoid: Contraindications - ANSWER-Systemic fungal infections
live viral vaccines
hsn to drug or components
Magnesium sulfate (MgSO4)
mineral/electrolyte: MOA - ANSWER-Replaces magnesium and maintains magnesium levels
Interferes with the release of Ach at the myoneural junction
Has a tocolytic effect of the vascular smooth muscle system by Suppressing automaticity in depolarized cells
having two effects:
◦interferes with calcium uptake in bronchial smooth muscle
◦interferes with acetylcholine release
Magnesium sulfate (MgSO4)
mineral/electrolyte: Indications - ANSWER-Refractory VF/VT with suspected hypomagnesemia (hx of alcoholism, malnutrition, protracted diarrhea)
Life threatening ventricular arrhythmias due to digitalis toxicity
Torsades
Control of seizures in PIH (eclampsia)
Adjunctive therapy in severe bronchospasm
Hypomagnesemia
Magnesium sulfate (MgSO4)
mineral/electrolyte: Dose - ANSWER-Can vary
CA/Torsades/Bronchospasm
2 g in 50 ml over 5-10 min
In cardiac arrest 2 g in 10 ml SIVP
Eclampsia (seizures in pregnancy)
loading dose of 4-5 g in 250 ml over 20 min or if no IV obtainable 10 g IM
maintenance infusion of 2 g/hr (2g in 1000 ml over 60 min)
Peds: for all
25-50 mg/kg IV over 10-30 min
For cardiac arrest 25-50 mg/kg in 10 ml SIVP
Magnesium sulfate (MgSO4)
mineral/electrolyte: Contraindications - ANSWER-Myocardial damaged pts
heart blocks
coma
Pregnant women in actively progressing labor
Magnesium sulfate (MgSO4)
mineral/electrolyte: Notes - ANSWER-Can cause flushing/sweating and higher doses can cause hypotension or with rapid administration
Use caution if pt has renal failure
Dimenhydrinate (gravol)
Anti-emetic, antivertigo, antihistamine: MOA - ANSWER-Inhibits nausea and vomiting by centrally depressing sensitivity to the labyrinth apparatus that relays stimuli to the chemoreceptor trigger zone and stimulates the vomiting center of the brain;
It also has some mild antagonism of muscarinic acetylcholine receptors in both the central and autonomic nervous system, which inhibits various signal transduction pathways
Dimenhydrinate (gravol)
Anti-emetic, antivertigo, antihistamine: Indications - ANSWER-Nausea, vomiting, dizziness assoc with motion sickness/vertigo
Meniere's disease
Dimenhydrinate (gravol)
Anti-emetic, antivertigo, antihistamine: Dose - ANSWER-Varies
25-50 mg SIVP
50-100 mg IM
Peds: 1.25 mg/kg IM to a max of 300 mg/day
Dimenhydrinate (gravol)
Anti-emetic, antivertigo, antihistamine: Contraindications - ANSWER-HSN to drug or benzyl alcohol
Any condition made worse by anti-cholinergic effects
newborns
Diphenhydramine HCl (Benadryl)
Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative): MOA - ANSWER-Antihistamine: competes for H1 receptor sites on smooth muscle of the bronchi, GI tract, uterus, and large vessels; by binding to these cellular receptors, it prevents access of histamine and suppresses histamine induced allergic symptoms (however they do not stop the RELEASE of H1)
Centrally acting anti-muscarinic actions of h1 blockade are responsible for the responsible for anti-vertigo/antiemesis
Antidyskinetic: Alleviates extraparmydal symptoms such as akathesia (RLS) as a result of using anti-dompaminergic medications
Diphenhydramine HCl (Benadryl)
Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative):
Indications - ANSWER-Allergic reaction/anaphylaxis
Dyskinesia from anti-psychotic/anti-emetic agents
Diphenhydramine HCl (Benadryl)
Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative):
Dose - ANSWER-25-50 mg IVP/IM/PO prn
peds: 12.5 mg - 25 mg IVP/IM/PO
Diphenhydramine HCl (Benadryl)
Anti-histamine, antivertigo, anti-emetic, anti-dyskinetic, sedative):
Contraindications - ANSWER-HSN
Acute asthma attacks
breast feeding
preterm and neonates as it can induce seizures
Dopamine Hcl (inotropin)
Adrenergic agonist, vasopressor, sympathomimetic
MOA - ANSWER-Immediate precursor to norepi, dopamine stimulates the dopaminergic bet-adrenergic and alpha-adrenergic receptors of the sympathetic nervous system
effects are very dose dependent
Dopamine Hcl (inotropin)
Adrenergic agonist, vasopressor, sympathomimetic
Indications - ANSWER-~Hemodynamically significant hypotension that is unresponsive to fluids
~cardiogenic shock
~hypotension assoc with bradycardia (chronotropic drugs infusions are recommended as an alternative to pacing in symptomatic unstable bradycardias)
~Maintain cardiac output during a ROSC period
Dopamine Hcl (inotropin)
Adrenergic agonist, vasopressor, sympathomimetic
Dose - ANSWER-5 mcg/kg/min - 20 mcg/kg/min titrated up by 5 until the desired effect
0.5- 3 mcg/kg/min has vasodilation effects in renal/mesentery/coronary/intracerebral vascular beds
5-10 mcg/kg/min has B1 receptor activation
10-20 mcg/kg/min has increased peripheral vasoconstriction (alpha effects)
Dopamine Hcl (inotropin)
Adrenergic agonist, vasopressor, sympathomimetic
Contraindications - ANSWER-Uncorrected tachydysrhythmias
VF/VT
Pheochromocytoma (can precipitate htn crisis)
Allergies to sulfites
MAO inhibitors
uncorrected hypovolemia (would essentially be useless if you squeeze the tank with no fluid)
do no mix with sodium bicarb
Droperidol (inapsine)
Tranquilizer
MOA - ANSWER-Produced marked sedation by directly blocking subcortical receptors; acts a potent D2 (dopamine receptor) antagonist with some histamine and serotonin antagonist activity
also blocks CNS receptors at the CTZ producing an anti-emetic effect
Droperidol (inapsine)
Tranquilizer
Indications - ANSWER-Acute psychotic episodes
-post operative nausea (hospital)
Droperidol (inapsine)
Tranquilizer
Dose - ANSWER-2.5 mg IM/SIVP repeated at 1.25 mg
enoxaparin sodium (lovenox)
Low molecular weight heparin
MOA - ANSWER-Anticoagulation action: LMWH that accelerates formation of antithrombin III-thrombin complex and deactivates thrombin preventing conversion of fibrinogen to fibrin.
enoxaparin sodium (lovenox)
Low molecular weight heparin
Use - ANSWER-Prevention of DVT and treatment of acute DVT Acute STEMI
enoxaparin sodium (lovenox)
Low molecular weight heparin
Dose - ANSWER-DVT: 1.5mg/kg/day or 1mg/kg twice/day SQ
Acute stemi: Acute STEMI when administered with TNK - 30mg IV bolus; then 1mg/kg SQ, maximum dose of 100mg SQ
enoxaparin sodium (lovenox)
Low molecular weight heparin
Contra-indications - ANSWER-Hypersensitivity to heparin or pork products
Active major bleeding
Acute or sub-acute bacterial endocarditis
Heparin or LMWH induced thrombocytopenia Suspected or known intracranial bleeding or spinal epidural hemorrhage
IV administration in patients >75 yrs of age
ephedrine
adrenergic; vasopressor
MOA - ANSWER-Ephedrine is both a direct and indirect acting sympathomimetic that stimulates alpha and beta adrenergic receptors. Release of norepinephrine from its storage sites is one of its indirect effects. In therapeutic doses, ephedrine relaxes bronchial smooth muscles and produces cardiac stimulation with increased systolic and diastolic blood pressure when norepinephrine stores aren't depleted.
Ephederine
Adrenergic, vasopressor
Indications - ANSWER-To correct hypotensive states (i.e. sepsis, spinal trauma, head injury, anaphylaxis) Note: Ephedrine can be given as a "bridge drug" (due to it short half life) until an inotropic / vasopressor infusion is started to maintain an adequate BP.
Ephederine
Adrenergic, vasopressor
Dose - ANSWER-Need to ask: What is the likelihood of Ischemic Heart Disease?
Low - 10 mg SIVP
Moderate - 7.5 mg SIVP
High - 5.0 mg SIVP
Give every 3-5 minutes until max dose of 50 mg or the desired effect is accomplished; duration of drug is approximately 15 min [Show Less]