Week 3 Pharmacology Flashcards
whats mannitol
- sugar-alcohol that is not effectively metabolized
- excreted largely unchanged in urine
whys mannitol used in emergency settings
lowers ICP when due to cerebral edema
when should you not use mannitol
crystals are present
what is the MOA of mannitol
pulls excess fluid from CNS into the vascular space Via osmotic gradietn
what are adverse rxns of mannitol
fluid overload (worsening HF, pulmonary edema, etc.)
renal failure
confusion
coma
sedation
whats the function of antiplatelet drugs
prevent platelet adhesion (needed to form thrombus)
ex. ASA (Aspirin), Clopidogrel (Plavix), Ticagrelor (Brilinta
ASA
- contraindicated in children due to Reyes syndrome
- pain relief properties not worthwhile in era of NSAIDS/acetaminophen
what modification was made to ASA due to its irritating effects
often enteric coated
what are the main indications for antiplatelet drugs?
treatment and prevention of MI/CVA
prevent in-stent re-thrombosis following angioplasty
why are antiplatelets often more beneficial than anticoagulant drugs?
lower bleeding rates
thrombolytic drugs
drugs that break down, or lyse, already formed clots
ex. Alteplase/TPA (Activase, Cathflo), Tenecteplase/TNK (TNKase)
whats the MOA of thrombolytic drugs
activate plasminogen and convert it to plasmin, which lyses the thrombus
what are the indications of thrombolytic drugs?
acute MI (STEMI)
arterial thrombolysis (DVT, PE)
acute ischemic stroke
blocked central line
what are adverse effects of thrombolytic drugs?
bleeding (internal, intracranial, and superficial)
N/V, HTN
hypersensitivity/anaphylactoid reactions
reperfusion cardiac dysrhythmias
what are some nurisng implications for thrombolytic drugs
- follow institutional guidelines for preparation and administration
- monitor IV sites for bleeding, redness, pain
- monitor bleeding from gums, mucous membranes, nose, and injection sites
- watch for signs of internal bleeding (decreased BP, restlessness, increased pulse, worsening neurological status)
antiepileptic drugs
- aka anticonvulsants
- single-drug therapy started before multiple-drug therapy tried to minimize adverse effects
- serum drug concentrations can be measured for some agents but do not correlate completely with efficacy or toxicity
what are the prominent goals of anticonvulsant therapy?
control/prevent seizures while maintaining a reasonable quality of life
minimize ADR and drug-induced toxicity
whats the MOA of anticonvulsants
unknown;
- `CNS depressants,
- reduce nerve’s ability to be stimulated,
- suppress transmission or speed of impulses from one nerve to the next
AEDs for analgesia (chronic neuropathic pain)
- carbamazepine (Tegretol)
- Gabapentin (Neurontin)
- Pregabalin (Lyrica)
AEDs used to treat psychiatric illness (used for bipolar depression)
- Carbamazepine (Tegretol)
- Lamotrigine (Lamictal)
- Valproic Acid, divalproex (Depakene)
gabaminergic vs glutaminergic
gaba- CNS depressants, ethanol, AEDs, others
gluta- stimulants, withdrawal of CNS depressants
whats the aim of balance for AEDs
slightly tip in a neuro-depressive manner by being gabaminergic
what can occur with virtually all AEDs
fatigue, cognitive impairment, dizziness, ataxia (cerebellar toxicity)
status epilepticus
a seizure >/ 30 min or 2 successive seizures without ful recovery in the same period
result:
hypotension, hypoxia, brain damage, possibly death
hydantoins; phenytoin
- non linear relationship between dose and drug levels for this agent (sim. to ethanol consumption)
- small dose titrations can produce larger than expected results
IV infusion of phenytoin
- irritating to veins
- slow directly into large vein through 20+-gauge venous catheter
- diluted in normal saline for IV infusion
- filter must be used
- max. rate must be used to avoid cardiac arrhythmias
- saline flush
what are considerations when taking phenytoin
same time each day w meals reducing GI upset
