gastric and duodenal ulceration (less GI problems than aspirin)
prolong gestation of labor
Class: Sympathetic agonist
Description: naturally occuring catecholamine; alph and beta adrenergic stimulant: more profound on beta receptors
Mech. of action: increase heart rate, increase cardiac contractile force, increased electrical activity, increase systemic vascular resistance, increase blood pressure, increased automaticity.
Onset: <2 min IV or ET
Peak: < 5 min IV/ET
Duration: 5-10 MIn IV/ET
Half Life: 5 min
Indications: Cardiac arrest( asystole, V-fib, pulsless v-tach, PEA) severe anaphylaxis, severe reactive airway disease.
Contraindications: Do not use 1:10000 unless resuscitative measures needed.
Precautions: protect from light, can be deactivated by sodium bicarb. flush line well between.
Side effects: palpitations, anxiety, tremors, headache, dizziness, nausea, vomiting. increases myocardial oxygen demand, only effective when o2 is adequate.
Interactions: ph dependent drug, deactivated by bicarb, and intesified in patients taking antidepressants.
Dosage: 1-10 000 IV, IO, ET
Adult arrest, 1.0 mg 3-5 min in tube increase by 2x
Child arrest, 0.01 mg/kg
Adult Severe anaphylaxis or asthma, use 1:10 000 IV @ 0.3-0.5 mg every 5-15 min
Child severe anaphylaxis or asthma use 1:10 000 @0.01 mg/ kg every 5-15 min
bone marrow depression
confusion (penetrate CNS)
dosage adjust: renal and liver disease
We can reduce toxicity via bone marrow stimulating factors.
Remember, this is due to ability to inhibit DNA synthesis
glycopeptide, blocks peptidoglycan polymerization, inhibit cell wall synthesis
toxicity-nausea, confusion, seizure, arrythmia, irritability
|Streptokinase ( Streptase)||
|SNS STIMULANTSCONJUNCTIVAL CONGESTION, IRRITATION, ALLERGIC CONDITONS||
CLASS: Adrenergic agonist, inotropid, vasopressor.
ACTION:Stimulates alpha & beta adrenergic receptor. At moderate doses (2 - 10mcg/kg/min), dopamine stimulate beta1 receptors, resulting in inotropy and increased cardiac output while maintaining dopaminergic-inducing vasodilatory effects. At high doses (>10mcg/kg/min), alpha adrenergic agonism predominates, & increased peripheral vascular resistance & vasoconstriction result.
INDICATION: Hypotension & decreased cardiac output associated with careodgenic shock & septic shock, hypotension after return of spontaneous circulation following cardiac arrest, symptomatic bradycardia, unresponsive to atropine.
ADVERSE: Tachycardia, arrythmias, skin & soft tissue necrosis, severe HTN from excessive vasoconstriction, angina, dyspnea, headache, N/V.
CONTRA: Pheochromocytoma, VF, VT, or other ventricular arrythmias, known sensitivity (including sulfites). Correct any hypovolemia with vol. fluid replacement beforeadministration.
Adult: 2 - 20mcg/kg/min IV,IO infusion. Starting slow dose 5mcg/kg/min; may gradually increase the infusion by 5 - 10mcg/kg/min to desired effect. Cardiac dose is usally 5 - 10 mcg/kg/min; vasopressor dose is usually 10 - 20mcg/kg/min.
Pediatric: Same as adult.
aminopenicillin, interfere with wall synthesis
most effective against gm-
-systemic or local
-one types: imidazoles
Class: Narcotic analgesic
Description: it is a central nervous system depressant and a potent analgesic. It has hemodynamic properties.
Mech of Action: A CNS depressant that acts on the opiate receptors in the brain, provides both analgesic and sedation. It increases peripheral venous capacitance and decreases venous return. This is called chemical phlebotomy. It also decreases myocardial oxygen demand. Can work in the treatment of pulmonary edema.
Onset: Immediate (IV) 15-30 min ( IM)
Peak: 20 min (IV) 30-60 min (IM)
Duration: 2-7 hours
Half life: 1-7 hours
Indications: Severe pain associated with MI, kidney stones pulmonary edema, burns.
Contraindications: not used in patients with volume depletion or severe hypotension and hypersensitivity to the drug, also do not use in patient with suspected head injury or abdominal pain.
Precautions: derivative of opium. highly addictive.It is a Schedule II drug. It can cause severe respiratory depression, narcan can be administered if needed.
Side Effects: Can cause nausea, vomiting, abdominal cramps, blurred vision, constricted pupils, altered mental status, headache and respiratory depression
Interactions: effects can be enhanced by antihistamines, antiemetics, sedatives, hypnotics, barbiturates and alcohol.
Dosage: Initsl dose is 2-10 mg IV, with additional doses of 2 mg every few min.
IM doses of 5-15 mg
can be given with an antiemetic for nausea and an increase in effect.
osmotic cathartics and irritant cathartics. Osmotic are more aggressive than bulk laxatives
-MUSCLE RELAXTANT- PO/IV- SPASTICITY FROM SEVERE DISORDERS LIKE MS/STROKE-HELPS WITH MALIGNANT HYPERTHERMIA CRISIS- CNS DEPRESSANT
|Fondaparinux: adverse effects and PK||
half life: 17-21 hrs
no monitoring needed
CLASS: Beta adrenergic antagonist, antianginal, antihypertensive, antiarrythmic class II
ACTION: Nonselective beta antagonist that binds with both the beta1 and beta2 receptors. Propranolol inhibits the strength of the heart's contractions, as well as HR. This results in a decrease in cardiac O2 consumption.
INDICATION: Aninga; narrow-complex tachycardia that originate from either a reentry mechanism (reentry SVT) or an automatic focus (junctional, ectopic, or multifocal tachycardia) uncontrolled by vagal maneuvers and Adenosine in pts with preserved ventricular function; AF and atrial flutter in pts with preserved ventricular function; HTN; migraine headaches.
ADVERSE: Bradycardia, AV block, bronchospasm, hypotension
CONTRA: Cardeogenic shock, heart failure, AV block, Bradycardia, PE, sick sinus syndrome, known sensitivity. Use with caution in chronic lung disease ( asthma and COPD)
Adult: 1 - 3mg IV, IO at a rate of 1mg/min; may repeat the dose 2 min later.
Pediatric: 0.01 - 0.1mg/kg slow IV IO over a 10 min period.
** Monitor BP and HR closely during admin**
anti tumor antibiotic
cell cycle non specific
inhibit RNA and DNA
|Nitroglycerin ( Nitrostat)||
Description: potent smooth muscle relaxant. can come in paste and spray
Mech Of Action: reduces cardiac work and dilates coronary arteries. Results in increased coronary blood flow and improved prefusion
Onset: 1-3 min(SL), 30 min (topical)
Peak: 5-10 min (SL), varies (topical)
Duration: 20-30 Min (SL), 3-6 hours (topical)
Half Life: 1-4 Min (SL),
Indications: Chest pain associated with angina pectoris, chest pain with MI, acute pulmonary edema without hypotension.
Contraindications: hypotensive and Increased ICP. Not for shock patients.
Precautions: tolerance can develop, headache is side effect, protect from light and monitoe BP closely
Side effects: headaches, dizziness, weakness, dry mouth, tachycardia, hypotension, orthostasis, skin rash, nausea, vomiting.
Interactions: severe hypotension with alcohol. Can cause orthostatic hypotension with beta blockers.
Dosage: (SL) 0.4 mg every 3-5 for 3 doses
also called 5-HT receptor antagonists. Ondansetron (Zofran)
|HIV protease inhibitors: mechanism||
decreases protease activity
decrease cleavage of viral GAG, GAG POL
decrease viral maturation, proliferation, and infectivity
decrease for death rate from AIDS
decrease HIV mRNA to minimally detectable levels (but virus still prolif. in CD4 cells)
Best works with RTI's families
|Epoetin alpha toxicities (how to reduce and mechanism of toxicity)||
seizures for those on dialysis
Due to rapid increase in Hb and Hct, so minimize by raising Hct slowly, monitoring and tx HTN.
|adverse effects: CV||
platelets- inhibition of activation, increased propensity for bruising, increased risk for hemorrhage
effect of cox 2 selective inhibitors- increase the risk of myocardial infarction and stroke esp. in patients at increased risk for CV disease
|pt comfort range w nitrous||
10-50% average 35%
|management of asthma||
traditional method- mild/mod stages (inhaled beta-2 agonist, oral theophylline)
-severe add oral glucocorticoid
newer method- use glucocorticoid from the start
|Describe how drugs usually leave a capillary to center the interstitial space in the tissue||
used in combination with anesthics to control the adverse effects of anesthetics
|foscarnet: mechanism of action||
inorganic phosphate analog compete with pyrophosphate binding site of viral polymeraseprevents cleave of pyrophosphate from triphosphates
inhibits DNA polymerase
prevents viral DNA synthesis
inhibits HIV reverse transcriptase (but too toxic for use)
|epoetin alpha (indications)||
anemia due to chronic renal failure
failure usually ue to concurrent iron deficiency
anemia due to other disorders
esp. with low serum EPO
anemia due to AZT in HIV pts
|NSAID toxicities: CV||
PGI2 is protective for vessel endothelium (synthesized by COX2)
inhibition of prostacyclin synthesis without inh. thromboxoane synthesis, you could promote increased platelet aggregation of endothelium that is detrimental
increase potential for MI and stroke (esp. COX2 agents)
alkalinizes ph of solution between 6 and 7
|The **** through which drugs act are normal points of control of physiologic processes (REPEAT)||
|Activated Charcoal, Kaolin/pectin, Bismuth||
Adsorbent makes other substances adhere to its outer surface, thus reducing the contact of that substance with the intestinal wall. Protectants cover the intestinal wall to form a physical barrier that protects the wall from contact with irritating or disease-producing compounds
|valacyclovir: mechanism, advantage over acyclovir||
mechanism- prodrug of acyclovir, so same mechanism after metabolism
has greater bioavailability, making it more advantageous for post herpetic neuralgia
|folate- storage, dietary sources, recommended intake||
storage- liver and other tissue
excretion- urine and stool
sources- green vegetables, yeast, liver, fruits
cooking can destroy 90% of folate'
recommended intake- 400 micrograms per day
if pregnant, lactating, 500-600
400 micrograms prevent NTD
study of SNP's and their role in determing an individuals pharmacokinetic (metabolism) and pharmacodynamic response to drugs
|PK's of sulindac||
prodrug (must be metabolized to active metabolite which is 500x more active than prodrug)
|emergency tx: emesis (purpose, success, CI)||
purpose- minimize further absorption of an ingested poison from GI tract
success depends on time since ingestion of poison and its rate of absorption
corrosive poison (ex: strong acid or alkali can cause gastric perforation or esophageal necrosis)
pertrolium distalate (aspiration pneumonia)
CNS stimulant (provoke convulsions)
|beta adrenergic agonist||
-act on BETA-2 receptors in airway smooth mm;
-cAMP to initiate mm relaxation
-oral or inhalation
problem: respiratory irritation/constriction; cardiac and cns stimulant
|How significant is the barrier to absorption when using the intramuscular route of administration?||
No significant barrier
|Amantidine: mechanism of action||
blocks viral M2 protein (an ion channel in viral membrane)
this leads to prevention of viral uncoating
|Compare the Nucleotide sequence between any two individuals||
nucleotide sequence between any two indivuals (not counting identical twins) is nearly identical at 99.5-99.9%
|Adverse effects: effects on renal system and CI's/cautions it leads to||
salt/water retention, so CI in:
chronic kidney disease
any state where activation of RAAS occurs
decrease effectiveness of antihypertensive meds
decreased urate excretion (esp. aspirin)
analgesic nephropathy- slowly progressive renal failure, decreasing concentrating capacity
associated with high doses of combinations of NSAIDS
associated with frequent UTI's
|emergency tx: ways to remove absorbed poison from body||
altered urinary pH
|side effects with anti-lipidemia drugs||
neuro and mm (myositis, myalgia, weakness, parasthesia)
liver toxicity, pancreatitis, blood dyscrasia, arrythmia
|NATURAL, USED PREOP TO REDUCE SALIVA AND GI SECRETIONS, BRADYCARDIA,||
CHOLINERGIC BLOCKING Dicyclomine (Bentyl)
|Role of CYP2D6 enzyme polymorphisms in various drugs and how a polymorphism interacts with different drugs. Give example||
remember a particular polymorphism does not treat all drugs equally
ex: you could have a poor metabolizer or ultra metabolizer of imipramine and need to dosage adjust, but that polymorphism has no effect on sertraline dosage
|Mechanism of antiinflammatory activity and chief clinical application||
by inhibition of PG production, but need larger doses
Ibuprofen: 400-800 mg every 6-8 hrs
analgesia/antipyretic- 200-400 mg every 4-6 hrs
Aspirin: 4-5 g per day (plasma levels 120-350 mcg/mL)
analgesia/antipyretic- 325-650 mg every 4-6 hrs (plasma levels less than 60 mcg/mL)
chief clinical application- pain and inflammation associated with musculoskeletal disorders
ONLY symptomatic relief (do not arrest the disease)
|danger of giving thalidomide in first trimester||
cause phocomelia (decrease size, absence of limbs) in children
|calcium channel blockers (class IV)||
prototype - Verapamil
decrease SA and AV node automaticity
decreases conductivity in through the AV node in Pt's with preserved ventricular funtion
|Fenanyl citrate(CNS) OPIOID ANALGESIC DRUGS||
- PROCEDURAL SEDATION OR ADJUNCTION TO GENERAL ANESTHSIA-RELIEVES MODERATE TO SEVERE PAIN(CANCER PAIN)
|Describe toxicity as it relates to dose scheduling||
minimal toxicity results to normal tissue along with maximal increase in mean survival time if you give a second dosage at day 7-8
before tumor cells recovery is complete
maximal toxicity would result if give a second dose after 2-3 days (at this point, normal tissue has not recovered)
|Name the two major advantages of the Po route over the IV,IM, SuBQ routes.||
Easy, convenient, inexpensive, safer than injection, Inducing emesis, inducing catharsis, preventing absorption into the blood
|Explain the importance of leucovorin rescue when administering MTX||
it is a form of tetrahydrofolate that allows us to bypass the inhibited DHFR caused by MTX
this will allow for an increase in MTX dosage which will increase tumor kill by allowing for:
enhanced formation of intratumoral MTX-polyglutamate (its active anti-tumor metabolite)
|IF I WERE TO GIVE YOU A LARGER DOSE OF A SEDATIVE-HYPNOTIC WHAT WOULD BE THE EFFECT||
SLEEP HYPNOTIC EFECT
|Iron poisoning: the impotance of period of apparent recovery in toxicity||
there is a point in "phase 2" of iron poisoning where the patient appears to approve
you must not send them home, and you must keep them for long term observation