Term
|
Definition
|
|
Term
|
Definition
| Block AT1 (angiotensin II subtype I) receptors, prevents constriction of arterioles. |
|
|
Term
| ACE-I (angiotensin converting enzyme inhibitor)effect; side effect. |
|
Definition
| decreases angiotensin levels, less sodium and water absorbed and lower blood pressure; increased bradykinin (inactivated by ACE), which also decreases bp thru NO release and vasodilation BUT is a PRO-inflammatory cytokine (irritation of lungs = cough) |
|
|
Term
|
Definition
|
|
Term
| Captopril and lisinopril, side effect? |
|
Definition
| only prils that aren't PROdrugs (which must be metabolized to activate); captopril contains S = allergic rxn and CAI, metallic/loss of taste, short half life (2-3 hr, others > 12 hr) |
|
|
Term
|
Definition
| ARBs (angiotensin II subtype I receptor blockers) |
|
|
Term
|
Definition
|
|
Term
| ACE-I and ARB side effects |
|
Definition
1) dry cough (increase bradykinin)
2)angioedema (vasodilation/serious if involves airways)
3)hyperkalemia (no Na resorbed, K remains in blood)
*all less common with ARBs |
|
|
Term
| ACE-I and ARB contraindications |
|
Definition
1) Bilateral renal artery stenosis i.e. low RPF (unilateral if only one functioning kidney)...start with low dose and monitor serum creatinin
2)hx of angioedema
3)pregnancy (fetal hypotension, malformations, renal failure, death) |
|
|
Term
| Added advantages of -prils (ACE-Is) |
|
Definition
1) cardioprotective (less stroke, MIs)
2) protection against diabetes and nephropathy associated with diabetes |
|
|
Term
| Drugs combined with -prils (ACEIs) and -sartans (ARBs) |
|
Definition
| other hypertension drugs (diuretic hydrochlorothiazide which decreases K; calcium channel blockers [with ACEIs] like verapamil which vasodilate arteries) |
|
|
Term
|
Definition
direct renin inhibitor
(like a beta 1 blocker: found in kidneys) |
|
|
Term
|
Definition
Loop
Thiazide
Potassium sparing
carboanhydrase inhibitor
xathine derivatives |
|
|
Term
| Which category of diuretic has a "high ceiling?" A "low ceiling?" |
|
Definition
High = Loop
Low = Thiazide |
|
|
Term
| Loop and thiazides are derived from this substance. |
|
Definition
| sulfonamide/H2NSO4 (except ethacrynic acid) |
|
|
Term
| Loop diuretics end in this suffix. |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| loop diuretic (that doesn't end in -semide) |
|
|
Term
|
Definition
| Loop diuretic (non-sulfonamide) |
|
|
Term
| Describes steps of loop diuretic action |
|
Definition
1) secreted in proximal tubules through PSOASS - Probenecid sensitive organic acid secretory system
2)Into the ascending loop of Henle
3) Inhibits Na/2Cl/K co-transport |
|
|
Term
| Endogenous negative organic acid that is secreted by PSOASS |
|
Definition
| Uric acid (PSOASS is saturable and so uric acid and exogenous secreted acids compete - > gout) |
|
|
Term
| Loop diuretic effects: urine volume? Renal O2 consumption? CSF production? Smooth muscle? Broncho- and vaso- effect? Carbonic anhydrase? RPF/GFR |
|
Definition
Up: Urine volume
Down: CSF, Renal O2 consumption (stops active reabsorption. CA Inhibited. RPF/GFR unchanged
Smooth muscle relaxation, Brocho- and vasodilation. |
|
|
Term
Loop diuetic effects: plasma K, Mg, Ca, Cl, Uric acid, glucose, TG, HDL, acid
SE? |
|
Definition
Down: K (arrhythmias, flat T, U waves), Mg, Ca (tx for hypercalcemia), Cl and H+ (hypochloremic alkalosis -> hypokalemia) , HDL
Up: uric acid, glucose, TG
SE: Cochlear ototoxicity (tinnitus) |
|
|
Term
|
Definition
For glaucoma (high IOP/intraocular pressure), ICP (intracranial pressure) , pulmonary edema, ARF (acute renal failure)
More for emergencies |
|
|
Term
|
Definition
| cardiac and renal insufficiency |
|
|
Term
| Chlorothiazide, Hydro-chlorothiazide |
|
Definition
|
|
Term
| Chlorthalidone and Indapamide |
|
Definition
| diuretics that act like thiazides but are not thiazides |
|
|
Term
| Describes steps of thiazide diuretic action |
|
Definition
1) secreted in early distal tubules through PSOASS - Probenecid sensitive organic acid secretory system
2) Inhibits Na/Cl co-transport |
|
|
Term
| Thiazide diuretic effects: urine volume? Carbonic anhydrase? RPF/GFR |
|
Definition
Up: urine volume (less than with loop diuretics)
Down: Urine volume in those with diabetes insipidus. Carbonic anhydrase (inhibited), RPF/GFR (don't use with ARF or as an IV) |
|
|
Term
Thiazide diuetic effects: plasma K, Mg, Ca, Cl, Uric acid, glucose, TG, HDL, acid
SE? |
|
Definition
Down: K (arrhythmias, flat T, U waves), Mg, Ca in urine, Cl and H+ (hypochloremic alkalosis -> hypokalemia) , HDL
Up: Ca (in plasma/conserves it), uric acid, glucose, TG |
|
|
Term
| Thiazine Diuretic oral uses |
|
Definition
| Cardiac insufficiency (reduce BP but low ceiling), edema, diabetes insipidus, urinary calculi composed of Ca salts. (COMBINE with K sparing diuretic to counter hypokalemia.) |
|
|
Term
| Aldosterone antagonists effect, mode of action |
|
Definition
| diuretic + potassium sparing thru less Na resorption; block aldosterone attachment to cytoplasmic receptors in collecting duct so no transporters synthesis. |
|
|
Term
| Spironolactone, Canrenone. Delivery method? t 1/2? SE? |
|
Definition
| Aldosterone antagonists: Spironolactone (oral only, 2 hr t1/2) Canrenone (IV, 17 hr t1/2); Steroidal side effects e.g. gynecomastia |
|
|
Term
| Cycloamidine derivatives effect, mode of action |
|
Definition
potassium sparing only;
1) secreted through Organic Cation Transporter into collecting duct
2) blocks Na channel and Na/H+ exchanger (mild increase in urine pH) |
|
|
Term
| Triamterene, Amiloride. Metabolism? t1/2? SE? |
|
Definition
| Cycloamidine derivatives, potassium sparing drugs, Only triamterene metabolized, Triamterene t1/2 = 4-6 hr, Amiloride 18-20 hr; Triamterene: decrease folic acid, Amiloride: increase plasma Ca, both: azotemia (increase nitrogen compounds) DO NOT COMBINE WITH other K sparing drugs (Aldosterone agonists, ACE inhibitors, supplements) |
|
|
Term
| Carbonic anhydrase inhibitors: functional group, effect, mode of action |
|
Definition
SO2NH2, pH in blood goes down, pH and K in urine (and urine volume/diuretic) go up, soda loses taste.
1)secreted into early proximal tubule through OAT
2)inhibition of CA |
|
|
Term
|
Definition
| for glaucoma (increased IOP), maintains respiratory drive (prevents mountain sickness-> hyperventilation, increased blood pH), sequential nephron blockade (of Na resorption) |
|
|
Term
|
Definition
| Carbo-anhydrase inhibitor |
|
|
Term
| Xanthine derivatives: mode of action, effect |
|
Definition
| adenosine receptor blocker (dilates efferent arteriole, raises RPF/GFR and thus water filtration (diuretic) |
|
|
Term
| Caffeine, theophylline, theobromine |
|
Definition
| xanthines (adenosine-1 receptor blockers) |
|
|
Term
| Action of PDEs (Phosphodiesterases) |
|
Definition
| break down of cAMP and cGMP |
|
|
Term
| Tissue localization of PDE3, PDE4, PDE5 and PDE6? |
|
Definition
| 3: heart, vascular smooth muscle; 4: lungs, mast cells, vascular smooth muscle; 5: corpus cavernosum, vascular smooth muscle and platelets; 6: retina |
|
|
Term
| xanthines mode of action, examples |
|
Definition
| unselective PDE inhibitors (in high doses), but mainly adenosine-1 receptor blockers; caffeine, theophylline, theobromine |
|
|
Term
| Adenosine receptors: A1? A2A? A2B? |
|
Definition
| Are are purinergic (activated by purines), activated A1 in heart lowers heart rate (xanthines block and raise HR), A2A: coronary artery vasodilation, A2B bronchiconstriction (not numerous enough to be affected by xanthines, unless asthmatic) |
|
|
Term
| Aminophylline, IV vs. oral? |
|
Definition
xanthine (block adenosine-1 receptors), unselective PDE inhibitor
IV for relief of acute asthma symptoms, oral to control asthma over time. |
|
|
Term
|
Definition
| Non-selective PDE-inhibition (cAMP and cGMP up causing smooth muscle relaxation and striated muscle contraction); adenosine receptor antagonist (HR up), increases catecholamine levels |
|
|
Term
| Xanthine PK metabolism? Inducers? Inhibitors |
|
Definition
| 1A2, inducers (clear faster): Smoke, high protein/low carbs, omeprazole (GERD, ulcer), barbiturates (sedative/seizure), carbamazepine (seizure), phenytoin (seizure), rifampin (orange color); Inhibitors (clear slower): high carbs/low protein, cimetidine (H2 blocker, stomach acid), Fluvoxamine (SSRI, anti-depressant), Quinolones, Macrolids (erythromycin) |
|
|
Term
| xanthine order of kinetics? side effects? |
|
Definition
| zero order above 35 microg/mL; tachyarrhythmia, nausea/vomiting, tremor, seizure, rhabdomyolysis (striated muscle damage) |
|
|
Term
| -rinones mode of action? effect? Examples |
|
Definition
| PDE III (cardiac) selective inhibitors. Increase cAMP and thus cardiac muscle contraction (increase HR/positive inotropes), also vasodilation (net O2 consumption/bp the same); ex: amrinone, milrinone, vesnarinone |
|
|
Term
|
Definition
| PDE III (cardiac) selective inhibitor |
|
|
Term
| -ilast mode of action, effect, examples |
|
Definition
| PDE 4 (lung) selective inhibitors, increase cAMP which reduces mast (inflammatory) cell activation in respiratory tract (for COPD) ex: cilomilast (Ariflo) |
|
|
Term
| -afil mode of action, effect, examples |
|
Definition
| PDE 5 (corpus cavernosum) selective inhibitor, increased blood flow to the penis (for ED), examples: sildenafil (Viagra), vardenafil (Levitra), tadalafil (Cialis) |
|
|
Term
| -afils side effects? metabolism? |
|
Definition
| sildenafil and vardenafil inhibit PDE 6 (retina, night blindness), tadalafil inhibits PDE 11 (skeletal muscle = back pain); mostly 3A4 (some 2C9) and excreted in feces |
|
|
Term
| Uses of cholinesterase inhibitors |
|
Definition
| Alzheimer's disease (symptom development reduction), reversal of NDMR (an anesthesia), Myasthenia gravis (disease with antibodies against Ach receptors) tx, Central Anticholinergic syndrome (dry as a bone..etc) tx |
|
|
Term
| Tacrine mode of action? Use? SE? |
|
Definition
| Non-specific cholinesterase inhibitor (AChE and BuChE = butyrylcholine found mostly in liver/periphery), Alzheimer tx. SE: Nausea, vomiting and liver damage (enzymes up) |
|
|
Term
| Donepezil mode of action and advantage? Use? Halflife? |
|
Definition
More selective ChEI (for ACh in the CNS) = less BuChE inhibition in periphery and less hepatoxicity. Alzheimer's tx
t1/2 = 70 hrs so once a day drug |
|
|
Term
| Rivastigmine mode of action, use? |
|
Definition
| AChE and BuChE inhibitor, Alzheimer's tx |
|
|
Term
| Tubocurarine mode of action, effect |
|
Definition
| Type of curare (isoquinoline alkaloids) that blocks ACh receptors (nicotinic) at neuromuscular junction, relaxation/paralysis of muscle |
|
|
Term
|
Definition
| Synthetic curare, muscle relaxation |
|
|
Term
| Malouetine, mode of action, effect |
|
Definition
| African aminosteroid that blocks neuromuscular junction, muscle relaxation |
|
|
Term
| 3 components of anesthesia |
|
Definition
| 1)analgesia like fentanyl 2)sedative like lorazepam 3)NDMR (non-depolarizing muscle relaxant) like pancuronium |
|
|
Term
|
Definition
| synthetic aminosteriod NDMR (non-depoloarizing muscle relaxant) |
|
|
Term
| Edrophonium mode of action, effect, advantage, SE?, reversal of its effect? |
|
Definition
| AChE inhibitor w/o CNS penetration, reversal of NDMR, fewer muscarinic effects than neostigmine and distribution terminates after 10 min (low potency); SE: Brochoconstriction, bronchospasm, bradycardia ... Note: don't use atropine to reverse, goes into CNS, use glycopyrrolate (muscarinic blocker w/o BBB penetration) |
|
|
Term
| Neostigmine, mode of action, effect |
|
Definition
| AChE inhibitor w/o CNS penetration, NDMR reversal (most potent/common) |
|
|
Term
| Myasthenia gravis drug types? |
|
Definition
| Immunosuppressants, steriods (reduce reactivity of immune system), AChE-Inhibitors...also thymectomy |
|
|
Term
| Methotrexate mode of action, use, drug interaction |
|
Definition
| immunosuppressant (low dose) = inhibitor of T cell activation and suppression of intercellular adhesion molecule expression, Myasthenia gravis tx; decreased excretion when used along with penicillin like antibiotics (renal tubular competition) |
|
|
Term
| cyclosporin A mode of action, use |
|
Definition
| immunosuppressant, binds to cyclophilin (immunophilin) of T-lymphocytes. This inhibits calcineurin which normally activates transcription of IL2; myasthenia gravis tx |
|
|
Term
| Pyridostigmine mode of action, use, SE? |
|
Definition
| AChE inhibitor w/o CNS penetration (more potent/long acting than other AChE inhibitors; first-line tx of Myasthenia gravis, preemptive tx before potential OP/nerve gas exposure; SE: can antagonize muscle relaxants (that block ACh receptors) |
|
|
Term
| Tacrolimus mode of action, use |
|
Definition
| immunosuppressant (calcineurin inhibitor like cyclosporin), myasthenia gravis tx (gradual reduction of anti-AChR antibodies) |
|
|
Term
| Organophosphates, toxic effects |
|
Definition
| Pesticides that inhibit AChE; DUMBBELLS (diarrhea, urination, mitosis, bronchorrhea, bronchospasm, emesis, lacrimation, laxation, salivation) |
|
|
Term
| Treatment of OP (organophosphate poisoning) |
|
Definition
| A FLOP (Atropine [anti-cholinergic], FLuid [atropine makes dry], Oxygen, Pralidoxime [removes OP from Cholinesterase, reactivates] |
|
|
Term
|
Definition
|
|
Term
| Physostigmine mode of action, use |
|
Definition
| Cholinesterase inhibitor that penetrates BBB. Used in ordeal by poison, counters Central Anticholinergeic Syndrome (mad as a hatter, dry as a bone, red as a beet, hot as a hare, blind as a bat). |
|
|
Term
| Random facts: K effects on digitoxicity, QRS widened in? Verapamil effect on ventricular arrhythmias? insulin inotropic effect? dopamine effect on renal perfusion? |
|
Definition
| hyperkalemia enhances acute, hypokalemia enhances chronic; QRS widened in ventricular arrhthymias, verapamil is counterindicated, slows heart/lowers bp w/o need; insulin most potent inotrope; low dose dopamine increases renal perfusion |
|
|
Term
| atropine (D/L-hyoscyamine), acts for how long? |
|
Definition
| muscarinic receptor blocker, 2 -3 days; tropicamide and phenylephrine preferred as mydriatics |
|
|
Term
| tropicamide mode of action, effect |
|
Definition
| shorter-acting cholinergeic antagonist (knocks out parasympathetic NS), mydriatic |
|
|
Term
| phenylephrine mode of action, effect |
|
Definition
| alpha adrenergic agonist/sympathomimetic; directly simulates iris dilator muscle - mydriatic |
|
|
Term
| muscarinic receptor blocker uses, overdose effect? |
|
Definition
| mydriasis, resuscitation (reduces PNS, takes break off heart), for secretions and bronchoconstriction (atropine - dries and opens airways), antidote for OP poisoning (use atropine - counters cholinergic SLUDGE: Salivation, lacrimation, urination, diaphoresis/hyperhidrosis, GI motility, emesis ALSO micropsia: see objects as smaller); overdose = Central Anticholinergic Syndrome (dry as a bone etc) |
|
|
Term
| Glycopyrrolate, distribution |
|
Definition
| muscarinic blocker w/o penetration of BBB/CNS (much weaker than atropine but no mad as a hatter), IV or oral (only 5% absorption) |
|
|
Term
| -tropium mode of action, use, examples with half life |
|
Definition
| Inhalative antimuscarinics (counters PNS brochoconstriction and secretion, for COPD/asthma, ex: Ipratropium and Oxitropium (short) and Tiotropium (long) |
|
|
Term
| Darifenacin mode of action, use, advantage |
|
Definition
| Selective M3 blocker (M3 receptor mediates detrusor contractility, also involved in bladder and gastrointestinal smooth muscle contraction, saliva production, iris sphincter function).; for urinary incontinence; advantage: won’t cause thirst |
|
|
Term
| Oxybutinin mode of action, use, advantage |
|
Definition
| Selective M3 blocker (but M3=M1), urinary incontinence; advantage: won't cause thirst |
|
|
Term
| Tolterodine mode of action, use, interesting fact |
|
Definition
| Non-selective muscarinic receptor blocker (uroselectivity not linked to one receptor sub-type; parotid effect down 8x), urinary incontinence |
|
|
Term
|
Definition
| Benadryl: 1st generation H1 blocker (sedation), alpha blocker, strong anticholinergic effect (muscarinic blocker) |
|
|
Term
|
Definition
| Methylated diphenhydramine: 1st generation H1 blocker, NMDA receptor antagonist, anticholinergic effect (2/3 of atropine, muscarinic blocker) |
|
|
Term
| Benzatropine, mode of action, effect, use |
|
Definition
| Atropine derivative, muscarinic blocker, counters ACh/dopamine imbalance due to reduced dopamine, for Parkinson disease |
|
|
Term
| Biperiden, mode of action, use |
|
Definition
| Tertiary amine and muscarinic blocker that reduces ACh, for Parkinson |
|
|
Term
| Trihexyphenidyl, mode of action, use |
|
Definition
| Tertiary amine and muscarinic blocker that reduces Ach, antiparkinson |
|
|
Term
|
Definition
| Muscarinic (metabotropic) receptor agonist with less central effect/BBB crossing than ACh |
|
|
Term
| Pilocarpine mode of action, use |
|
Definition
| Non-selective M3 agonist, for chornic open-angle and acute angle-closure glaucoma (increased aqueous outflow) |
|
|
Term
| Cevimeline, mode of action, effect, use |
|
Definition
| Selective M3 agonist, increased secretion of saliva and tears; for dry mouth and especially for chronic dry eyes/mouth from Sjogren's syndrome |
|
|
Term
| How does NO act to relax smooth muscle? |
|
Definition
| activates guanylate cyclase, which produces cGMP (which is broken down by PDE). cGMP activates protein kinase that prevents release of Ca from ER, leading to muscle relaxation. |
|
|
Term
|
Definition
|
|
Term
| Nitroglycerin mode of action, effect/use |
|
Definition
| NO donor, for acute angina, also reduces bp (dose dependent), requires sulfhydryl-containing cysteine -> depletion of cysteine = nitrate tolerance. |
|
|
Term
|
Definition
| Treatment of angina and cyanide poisoning (by creating methemoglobin which sequesters cyanide as non-toxic cyanomethemoglobin. Methemoglobin converted back to hemoglobin by methylene blue). Also illegal inhalant that produces euphoria (poppers). |
|
|
Term
| isosorbide mononitrate and dinitrate |
|
Definition
| NO donor with longer t1/2's (5 hrs/1 hr) than nitroglycerin (minutes, need expensive patches) |
|
|
Term
| nicorandil, effect, arrhythmias? side effects? |
|
Definition
| NO donor (increases cGMP) and K-channel opener (hyperpolarizes cell), arterial and venous relaxation/dilation; doesn't cause arrhythmias because is selective of vascular potassium channels (no opening of cardiac or pancreatic channels); mouth ulcers |
|
|
Term
| Ranolazine mode of action, effect |
|
Definition
| indirectly reduces available Ca in cardiac muscle by altering the transcellular late Na current which affects sodium dependent calcium channels, relaxes heart muscle and reduces cardiac ischemia (lack of O2) |
|
|
Term
| Trimetazidine mode of action, effect |
|
Definition
| shifts cardiac metabolism from fatty acid beta oxidation toward glucose oxidation reducing O2 consuption, relaxes cardiac muscle/cardioprotective |
|
|
Term
| Ivabradine mode of action, effect |
|
Definition
| Inhibits sinus node pacemaking current (enhanced PNS effect), slows heart rate without side effects of beta-1 blockers (reduced contractility) and beta-2 blockage (prevention of bronchodilation) |
|
|
Term
| DON'T use NO donors with these drugs |
|
Definition
| PDE 5 inhibitors like sildenafil (also relax smooth muscle, take off nitrates for the day), alpha-1 blockers (block constriction of blood vessels and reduce bp like NO donors) |
|
|
Term
| Main target of anesthetics? |
|
Definition
|
|
Term
| Measure of volatile anesthesia potency? Meaning of it? |
|
Definition
| Minimum alveolar concentration (MAC); the alveolar concentration of an anesthetic that prevents movement of 50 percent of the subjects in response to pain. |
|
|
Term
| Mechanism of action of inhaled anesthetics; relationship between solubility and inhaled anesthetics? |
|
Definition
| agonize GABA receptor (most) or antagonize NMDA (N2O) also: molecules dissolve in lipid cell membrane and influence cell's ability to depolarize by distorting the channels necessary for ion flux; correlation between lipid solubility and MAC (minimum alveolar concentration) |
|
|
Term
| Halothane use, structure, metabolism % (higher is worse), blood/gas coefficient (speed of action: higher is slower); side effects |
|
Definition
| inhaled anesthetic; alkane; 20%; 2.3; malignant hyperthermia (caused only by anesthetics) and halothane hepatitis (due to antibodies to metabolite trifluoroacetate) |
|
|
Term
| Enflurane use, structure, metabolism % (higher is worse), blood/gas coefficient (speed of action: higher is slower); side effects |
|
Definition
| inhaled anesthetic; ether; 2%; 1.8; increased seizure risk |
|
|
Term
| Isoflurane use, structure, metabolism % (higher is worse), blood/gas coefficient (speed of action: higher is slower) |
|
Definition
| inhaled anesthetic; ether; 0.2%; 1.4 |
|
|
Term
| Sevoflurane use, structure, metabolism % (higher is worse), blood/gas coefficient (speed of action: higher is slower); side effects |
|
Definition
| inhaled anesthetic; ether; 4% (but still popular because rapid onset/offset -> 0.59; reacts with CO2 to form Compound A which causes kidney damage |
|
|
Term
| Desflurane use, structure, metabolism % (higher is worse), blood/gas coefficient (speed of action: higher is slower); advantage? |
|
Definition
| inhaled anesthetic; ether; 0.04%; 0.42 (ultra rapid onset); rapid elimination and awakening (unlike halothane which requires ventilation with O2 for 5 min after use) also: resistant to lime soda degradation (soda lime is used to absorb exhaled CO2 but can degrade anesthetics into toxic products) |
|
|
Term
| Nitrous Oxide (N2O) use, mode of action, metabolism % (higher is worse), blood/gas coefficient (speed of action: higher is slower); side effects |
|
Definition
| inhaled anesthetic; NMDA antagonist; 104% metabolism (different mode of action); 0.4 (fast acting); sympathomimetic, inhibits B12 and B12 enzymes which participate in myelin and RBC production |
|
|
Term
| Succinyl-choline (SUX) mode of action, effect |
|
Definition
| prevents Na channel at neuromuscular junction from closing (attaches at both alpha subunits and opens channel but broken down slowly by ACh esterase); paralysis |
|
|
Term
| Percent of succinyl-choline (SUX) metabolized by plasma ChE (BuChE)? metabolism of SUX vs. ACh by AChE at neuromuscular junction? |
|
Definition
| 90-99% (only 1-10% reaches target); SUX: 2-7 min (time of action) vs. ACh: milliseconds |
|
|
Term
| TOF? Use? Result with DMR (SUX)? Result with NDMR? |
|
Definition
| Train of four impulses to ulnar nerve (causes thumb to adduct in plane perpendicular to palm); used to monitor extent of muscle relaxation; With SUX: amplitude of each response decreases equally; With NDMR: each subsequent response is less than previous response (fades) |
|
|
Term
| Succynl-choline use, onset/half life, side effects |
|
Definition
| muscle relaxant portion of anesthesia used for intubation; rapid onset (60 sec) and ultra short acting (3 min: too short for hypoxia to cause brain); fasciculations (muscle twitches) that lead to myalgia (muscle pain) esp. in young females, and increased pressure (intra -cranial, -gastric, -ocular), bradycardia and brochospasm (Cholergic effect/give glycopyrrolate), hyperkalema (squeezes cells; +0.5 mmol/L; higher with muscle disease and burns), masseter muscle spasm (warning sign of -> malignant hyperthermia also caused by halothane (treat with dantrolene and hyperventilate) |
|
|
Term
| Atypical BuChE (plasma ChE) effect, SUX duration if no ChE? test? |
|
Definition
| longer duration of SUX and other drugs degraded by esterases (remifentanil: mu opiod agonist; mivacurium: NDMR; cocaine: ester LA; esmolol: beta blocker); SUX 3 min -> 12 hr if no ChE; Dibucaine test (normal: 80% inhibition of ChE; atypical: 20% (homozygotes), 40-60% heterozygotes. |
|
|
Term
| Clopidogrel mode of action? effect? use? metabolism? caveat? brand name? Other similar drug? |
|
Definition
| metabolized by liver into active metabolites that bind to P2Y12 receptor of platelets and reduce aggregation; increased blood flow through narrowed vessels; standard of care for MI/CAD (a better asprin); 85% metabolized by plasma ChE, so atypical ChE will cause longer duration/excessive bleeding; brand name: Plavix; Prasugrel |
|
|
Term
| NDMR (Nondepolarizing Muscle Relaxant) mode of action, effect, advantage; Don'ts |
|
Definition
| binds to alpha subunit of nicotinic receptor at neuromuscular junction and prevents Na channel from opening; muscle relaxation and paralysis; no fasciculations or myalgia like SUX; Don't use if patient is awake or not intubated |
|
|
Term
|
Definition
| Isoquinolines (South American, curare/tubocurarine like) and Aminosteroids (African, malouetine like) |
|
|
Term
|
Definition
| first synthetic isoquinoline/curare like NDMR |
|
|
Term
|
Definition
| first synthetic aminosteroid/malouetine like NDMR |
|
|
Term
|
Definition
| ending for isoquinoline NMDRs |
|
|
Term
| Isoquinoline NMDR side effects? |
|
Definition
| Histamine release -> tachycardia (bad if CAD) and brochoconstriction (bad if asthma/COPD) |
|
|
Term
|
Definition
| ending for aminosteroid NMDR |
|
|
Term
| Aminosteroid NMDR side effect? |
|
Definition
| vagolytic (inhibit vagus nerve) -> increased heart rate and bronchodilation |
|
|
Term
| Pancuronium use, metabolism, duration, side effect? |
|
Definition
| Aminosteroid NMDR; hepatic and renal; long acting (60-90 min); pronounced tachycardia (most vagolytic) |
|
|
Term
| Pipecuronium use, metabolism, duration? |
|
Definition
| Aminosteroid NMDR; hepatic and renal; long acting (90-120 min) |
|
|
Term
| Vecuronium use, metabolism, duration? |
|
Definition
| Aminosteroid NMDR; kindney/renal/bile; intermediate acting (30-40 min: popular b/c duration of many procedures) |
|
|
Term
| Rocuronium use, metabolism, duration? |
|
Definition
| Aminosteroid NMDR; renal/bile only; intermediate acting (30-40 min) |
|
|
Term
| Mivacurium use, metabolism, duration, side effect? |
|
Definition
| isoquinoline NMDR; plasma ChE; shortest acting NMDR(5-15 min: but long enough to cause brain damage due to hypoxia) |
|
|
Term
| Atracurium use, metabolism, duration, side effect? |
|
Definition
| isoquinoline NMDR; 1/3 Hofmann (spontaneous) degradation, rest plasma esterases; intermediate duration (20 min: because some hepatic metabolism); laudanosine production (hepatic metabolite that stimulates CNS [NMDA agonist/GABA antagonist], can lead to seizures) |
|
|
Term
| Cisatracurium use, metabolism, duration, side effect? |
|
Definition
| isoquinoline NMDR; partial Hofmann (spontaneous) degradation, partial plasma esterases; intermediate duration (30 min: because some hepatic metabolism); laudanosine production (hepatic metabolite that stimulates CNS [NMDA agonist/GABA antagonist], can lead to seizures) |
|
|
Term
| Doxacurium use, metabolism, duration? |
|
Definition
| isoquinoline NMDR; not metabolized/renal elimination; long duration (120 min: use this or pipecuronium) |
|
|
Term
|
Definition
|
|
Term
| Rate limiting step of cholesterol synthesis |
|
Definition
| HMG-CoA reductase (Hydroxy-Methyl-Glutaryl CoA reductase: HMG CoA to Mevalonate) |
|
|
Term
| Lipophilic statins mode of action, effect, examples |
|
Definition
| Diffuse freely through cell membrane of hepatocytes, inhibit HMG-CoA reductase, which reduces cholesterol in cell, which triggers the sterol sensing domain of ER to move to Golgi where SREBP (sterol regulating element binding protein) is freed. This activates genes for LDL receptors that increase LDL/cholesterol re-uptake from blood vessels, ex: lovastatin, simvastatin, fluvastatin, atorvastatin |
|
|
Term
| Pleiotropic effects of statins |
|
Definition
| Helps to treat osteoporosis, cancer, Alzheimer's Disease and Multiple sclerosis |
|
|
Term
|
Definition
| When isoprenoids (intermediate product of cholesterol syntheses down stream of HMG CoA and mevalonate) bind to G-proteins like Rho/Ras, they are brought to cell membrane and activated. Statins reduce isoprenoid and thus G-protein activation. |
|
|
Term
| Formation of atherosclerotic plaque mechanism |
|
Definition
| Diabetes, high cholesterol and high bp damage endothelium of vessel, lipids leak in and are oxidized attracting monocytes that invade endothelium (sub-epithelium) and become macrophages that grow and become foam cells. Smooth muscle cells also proliferate further narrowing lumen, plaque breaks open, clot forms, clot released into blood stream. |
|
|
Term
| How do statins prevent endothelial dysfunction? |
|
Definition
| Statins reduce monocyte adherence to endothelium, reduce MMP (matrix metaloproteases) used by macrophages to move through endothelium (increasing plaque stability), increase collagen (increasing plaque stability), decrease Rho/Ras prenylation and activity (which decreases smooth muscle cell proliferation and stenosis), blocks production of mevalonate which usually inhibits production of NO. Increased NO dilates vessel. |
|
|
Term
| Action of statins on osteoclasts |
|
Definition
| Statins block formation of isoprenoids Geranylgeranyl PP and Farnesyl PP (also blocked by N-containing bisphosphonates), which prenylate Rho protein that promotes ruffled border of osteoclasts, which is necessary for bone breakdown. |
|
|
Term
|
Definition
| Lovastatin, simvastatin, pravastatin (from fungus) |
|
|
Term
|
Definition
| Atorvastatin (Lipitor), fluvastatin, rosuvastatin...cerivastatin removed from market due to drug interaction with fibrates |
|
|
Term
| Hydrophilic statins mode of action, effect, examples, advantages over lipophilic statins?? |
|
Definition
| Move through OATs (organic acid transporters) of membrane of hepatocytes, inhibit HMG-CoA reductase, which reduces cholesterol in cell, which triggers the sterol sensing domain of ER to move to Golgi where SREBP (sterol regulating element binding protein) is freed. This activates genes for LDL receptors that increase LDL/cholesterol re-uptake from blood vessels, ex: pravastatin, rosuvastatin; higher FPE, lower bioavailability, can't diffuse into other cells |
|
|
Term
|
Definition
|
|
Term
| Statin not metabolized by CYP450 enzyme? CYP450 enzyme that metabolizes most statins? Statins metabolized by 2C9? Excretion? |
|
Definition
| Pravastatin; CYP450 3A4 (beware of inhibitors like grapefruit juice and cimetidine); Fluvostatin and Rosuvastatin by 2C9. Excreted through feces. |
|
|
Term
|
Definition
| Natural, hydrophilic statin, not metabolized by CYP450 enzyme, with only 50% protein binding (bad, frees to move throughout body) but uses liver specific OAT, so cancels possible negative effect. |
|
|
Term
| Statins with long half lifes (>3 hr) |
|
Definition
| Atorvastatin and Rosuvastatin (greatest effect on HDL-cholesterol and TGs too) |
|
|
Term
|
Definition
| Decreased LDL-cholesterol (Also smaller decrease in TG and small increase in HDL-cholesterol especially atorvastatin and rosuvastatin) |
|
|
Term
|
Definition
| hepatotoxicity (dose-related elevated serum transaminases in minority of users), rhabdomyotoxicity (myalgia -> myopathy with elevated CK [creatin phosphokinase] levels -> rhabdomyolysis with myoglobinemia [clogs glomerulus] & myoglobinuria [tea-colored]); increases K = hyperkalemia and cardiac arrhythmias |
|
|
Term
| Risk factors for statin-induced myotoxicity |
|
Definition
| -dose, use of other CYP450 (3A4 & 2C9) metabolized drugs, use of other drugs that produce myotoxicity like fibrates, theoretically lipophilic statins are worse |
|
|
Term
|
Definition
| Pregnancy (FDA category X), active chronic liver disease |
|
|
Term
| Phentolamine, mode of action, effect, use, avoid? |
|
Definition
| Non-selective alpha receptor blocker, causes vasodilation and drop in bp, emergency use for very high blood pressure that includes non-functional precapillary sphincters, leading to edema seen in pheochromocytoma (catecholamine secreting tumors); avoid beta blockers to lower bp (with cocaine induced HTN too) because opens constricting alpha receptors to increased catecholamines. |
|
|
Term
| Effect of overstimulation of alpha receptor? |
|
Definition
| Acute urine retention due to G protein activation, leading to increase IP3 and DAG, leading to increase in cytosolic Ca. |
|
|
Term
| Alpha-1A receptor blocker effect? Type of Alpha-1 receptors in prostate? |
|
Definition
| Called uroselective blockers, used for relief of lower urinary tract symptoms (LUTS) due to bladder outlet obstruction (BOO) and Benign Prostatic Hypertrophy (BPH); 70% alpha receptors in prostate are alpha 1A, rest 1D. |
|
|
Term
| Doxasosin mode of action, selectivity, use, side effects, derived from? |
|
Definition
| selective alpha 1 blocker but non-uroselective; used for BPH symptoms; SE: orthostatic hypotension; quinozoline derivative |
|
|
Term
| Terazosin mode of action, selectivity, use, side effect, derived from? |
|
Definition
| selective alpha 1 blocker but non-uroselective; used for BPH symptoms; SE: orthostatic hypotension; quinozoline derivative |
|
|
Term
| Alfuzosin mode of action, use, selectivity, use, derived from |
|
Definition
| selective alpha 1 blocker and fuctionally uroselective (more selective for alpha 1A than other drugs; used for BPH symptoms; quinozoline derivative |
|
|
Term
| Tamsulosin mode of action, use, selectivity, use, derived from, brand name |
|
Definition
| selective alpha 1A blocker and uroselective; used for BPH symptoms; sulfone-methyl-amine derivative, Flomax |
|
|
Term
| Silodosin mode of action, use, selectivity, use, advantage, brand name |
|
Definition
| selective alpha 1A blocker and highly uroselective; used for BPH symptoms; No orthostatic hypotension (lack of effect in vasculature); Rapaflo |
|
|
Term
| How are alpha 1 selective but non-uroselective drugs marketed? |
|
Definition
| To lower BP and address BPH symptoms in older males. |
|
|
Term
| alpha 2 receptors location? controls? effect? side effects? |
|
Definition
| Presynaptic; controls neurotransmitter release; shuts down sympathetic nervous system (analgesia and sedation); SE: dry mouth and parotid pain |
|
|
Term
| imitazol 1 receptors location? controls? effect? side effects? |
|
Definition
| Presynaptic; controls neurotransmitter release; shuts down sympathetic nervous system/allows parasympathetic NS to dominate (lowers bp); SE: bradycardia, constipation (strange because not parasympathetic effect), water retention (co-administer diuretic). |
|
|
Term
| clonidine and clonidine-like drugs mode of action |
|
Definition
| centrally acting alpha 2 and imidazoline 1 receptor agonists |
|
|
Term
|
Definition
| selective alpha 1 blocker |
|
|
Term
| alpha-methyldopa mode of action, use |
|
Definition
| centrally acting alpha 2 selective agonist (also a competitive inhibitor of DOPA decarboxylase which reduces production of all catecholamines lowering sympathetic effects in peripheral NS) aka clonidine-like; and used to lower bp during pregnancy (category B) |
|
|
Term
| clonidine mode of action, use, side effect? ending |
|
Definition
| centrally acting agonist at both alpha 2 and imadazoline receptors; lowers bp; as IV some activation of alpha 1 receptors = vasoconstriction; -nidine or -midine except methyldopa |
|
|
Term
| dex-medetomidine mode of action; use |
|
Definition
| centrally acting alpha 2 agonist only; sedative anxiolytic (antianxiety) w/o respiratory depression |
|
|
Term
| moxonidine mode of action, effect; use |
|
Definition
| centrally acting, selective imidazoline 1 receptor agonist ;decreases sympathetic nervous system activity; used to lower bp |
|
|
Term
| clonidine-like drug side effects? |
|
Definition
| sedation, dry mouth and nasal mucosa, bradycardia, orthostatic hypotension, impotence, constipation/nausea/gastric upset, fluid retention and edema (concurrent thiazide diuretic necessary), rebound hypertension |
|
|
Term
| Peripherally acting alpha 1 receptor agonist uses |
|
Definition
| for hypotensive states (vasoconstriction), as a mydriatic (pupil dilation), nasal decongestant (constricts capillaries in sinuses) |
|
|
Term
| oxymetazoline mode of action, use |
|
Definition
| peripheral alpha 1 agonist; nasal decongestant |
|
|
Term
| xylometazoline mode of action, use |
|
Definition
| peripheral alpha 1 agonist; nasal decongestant and mydriatic |
|
|
Term
| phenylephrine mode of action, use, brand name |
|
Definition
| peripheral alpha 1 agonist; nasal decongestant, Sudafed |
|
|
Term
| norepinephrine mode of action, effect, overdose effect? |
|
Definition
| more selective as alpha receptor agonist; vasoconstriction; have a bp but not perfusion |
|
|
Term
| ephinephrine mode of action, effect |
|
Definition
| more selective as beta receptor agonist; inotrophic |
|
|
Term
| alpha 1 agonist side effects? Suggested use? |
|
Definition
| headache, reflex bradycardia, excitability and restlessness, increased afterload (work of heart), angina if coronary artery disease, nasal decongestant rebound effect: receptor reuptake. ALSO: nasal vasoconstriction -> systemic uptake -> systemic vasoconstriction -> acidosis -> vasodilation (causes headache); Don't use continuously |
|
|
Term
| beta 2 receptor agonist PD, effect, uses |
|
Definition
| increase cAMP by activating Gs protein which decreases cytosolic Ca...also decreases histamine and LT release; relaxes smooth muscle and mild anti-inflammatory; for asthma (COPD), uterus relaxation (delays birth/also use Mg), hyperkalemia (squeezes K into cell, insulin/dextrose is first-line tx) |
|
|
Term
|
Definition
| beta 2 agonists, smooth muscle relaxation |
|
|
Term
| Albuterol mode of action, onset/offset, use, side effect, secretion, good guy: R/S isomer? |
|
Definition
| beta-2 agonist; rapid onset/short acting (ROSA); asthma reliever (2-4 hr); tachycardia (some beta 1 action); renal secretion; R = eutomer, more affinity for beta 2 than distomer (L) |
|
|
Term
| levalbuterol mode of action, onset/offset, use, side effect |
|
Definition
| only eutomer version of albuterol beta-2 agonist; rapid onset/short acting (ROSA); asthma reliever (2-4 hr); less tachycardia (more selective for beta 2 than beta 1 than albuterol) |
|
|
Term
| ROSA beta 2 agonists, use |
|
Definition
| bambuterol -> terbutalin, fenoterol, reproterol, pirbuterol, bitolterol -> colterol (slow onset); asthma relievers (2-4 hr) |
|
|
Term
| Long acting beta 2 agonists, use, current trend? |
|
Definition
| salmeterol, formoterol; asthma controllers (> 10 hr), move toward anti-inflammatory steroids as controllers |
|
|
Term
| Salmeterol mode of action, use, onset/offset |
|
Definition
| partial beta 2 agonists, asthma controller, slow onset/long acting (SOLA) |
|
|
Term
| Formoterol mode of action, use, onset/offset |
|
Definition
| beta 2 agonist; asthma controller OR reliever; rapid onset/long acting (ROLA) |
|
|
Term
| beta 1 receptor agonist PD, effect |
|
Definition
|
|
Term
| dobutamine mode of action, effect, synthetic version of? |
|
Definition
| pseudo beta 1 agonist (alpha 1 agonist and antagonism of racemic mix cancel); inotropic used by surgeons; synthetic catecholamine |
|
|
Term
| dopamine dose effects: low, medium, high? |
|
Definition
| Low (D1) = renal dose, dilates renal vasculature, increased RPF/perfusion; medium (beta 1) = heart dose, increased heart rate; high (alpha 1) = increased vasoconstriction, afterload and oxygen consumption. |
|
|
Term
| dopexamine mode of action, effect, use, synthetic version of? |
|
Definition
| D1 and beta 2 agonists at low dose, decreases afterload (vasodilation) and O2 consumption, inotropic; synthetic catecholamine (dopamine) |
|
|
Term
| fenoldopam mode of action, use, equivalent to? |
|
Definition
| selective D1 agonist; anti-hypertensive; like low dose dopamine (renal dose) |
|
|
Term
| Isoprenaline mode of action, effect, synthetic version of? |
|
Definition
| non-selective beta agonist; inotropic and vasodilation/decrease afterload (increase in O2 consumption more moderate like PDE III inhibitors); synthetic catecholamine |
|
|
Term
|
Definition
| Intrinsic sympathomimetic activity; less likely to overdose on beta blockers with this (blockers also partial agonists), no increase in TG, LDL or glucose |
|
|
Term
| selective beta 1 blockers effect, at high doses,examples? |
|
Definition
| slow heart without vascular effect; lose selectivity at high doses; metaprolol, atenolol, acebutolol |
|
|
Term
| Beta blocker effect, side effects? for overdose? |
|
Definition
| vasodilation; loss of ability to vasodilate (bad for asthma and COPD), increased TG, LDL and glucose (like diuretics), dreams if fat soluble (ex: diuretic propranolol); use inotropic insulin or glucagon for overdose |
|
|
Term
| propranolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| non-selective beta and Na channel blocker; fat soluble (dreams); Hepatatic 1A and 2D6; no ISA |
|
|
Term
| pindolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| non-selective beta and (membrane stabilizing) Na channel blocker, 5HT1a agonist; water soluble; renal excretion; strong ISA |
|
|
Term
| metoprolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| selective beta 1 blocker; fat soluble (dreams); hepatic 2D6; no ISA |
|
|
Term
| atenolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| selective beta 1 blocker; water soluble; renal elimination; no ISA |
|
|
Term
| acebutolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| selective beta 1 and membrane stabilizing Na channel blocker; fat soluble; renal elimination; ISA (also less effect on metabolic profile TG, LDL) |
|
|
Term
| nadolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| non-selective beta blocker; water soluble; renal excretion; no ISA |
|
|
Term
| Water soluble beta blockers? |
|
Definition
| PANS: pindolol, atenolol, nadolol, satalol |
|
|
Term
| esmolol mode of action, delivery?, metabolism? half life? |
|
Definition
| beta blocker; IV, plasma esterases; ultra short acting |
|
|
Term
| beta blockers affect on cardio depolarization |
|
Definition
| Mainly flattens phase 4 (harder to depolarize) |
|
|
Term
| labetalol mode of action, effect, |
|
Definition
| mixed: non-cardio selective alpha/beta blocker and more; mainly reduces afterload and bronchoconstriction (alpha blocker) |
|
|
Term
| carvedilol mode of action, effect |
|
Definition
| mixed non-cardioselective alpha/beta blocker; stops vasculature from contracting (alpha blocker) |
|
|
Term
| Nebivolol mode of action, metabolism |
|
Definition
| beta blocker with NO (an EDRF) potentiating effect; metabolism by 2D6 to active moieties. NOTE EDRF = endothelium derived relaxing factor |
|
|
Term
| For beta blocker overdose? |
|
Definition
| Use inotrope insulin or glucagon (can't use beta agonist because receptor blocked) |
|
|
Term
| beta 2 receptor agonist PD, effect, uses |
|
Definition
| increase cAMP by activating Gs protein which decreases cytosolic Ca...also decreases histamine and LT release; relaxes smooth muscle and mild anti-inflammatory; for asthma (COPD), uterus relaxation (delays birth/also use Mg), hyperkalemia (squeezes K into cell, insulin/dextrose is first-line tx) |
|
|
Term
|
Definition
| beta 2 agonists, smooth muscle relaxation |
|
|
Term
| Albuterol mode of action, onset/offset, use, side effect, secretion, good guy: R/S isomer? |
|
Definition
| beta-2 agonist; rapid onset/short acting (ROSA); asthma reliever (2-4 hr); tachycardia (some beta 1 action); renal secretion; R = eutomer, more affinity for beta 2 than distomer (L) |
|
|
Term
| levalbuterol mode of action, onset/offset, use, side effect |
|
Definition
| only eutomer version of albuterol beta-2 agonist; rapid onset/short acting (ROSA); asthma reliever (2-4 hr); less tachycardia (more selective for beta 2 than beta 1 than albuterol) |
|
|
Term
| ROSA beta 2 agonists, use |
|
Definition
| bambuterol -> terbutalin, fenoterol, reproterol, pirbuterol, bitolterol -> colterol (slow onset); asthma relievers (2-4 hr) |
|
|
Term
| Long acting beta 2 agonists, use, current trend? |
|
Definition
| salmeterol, formoterol; asthma controllers (> 10 hr), move toward anti-inflammatory steroids as controllers |
|
|
Term
| Salmeterol mode of action, use, onset/offset |
|
Definition
| partial beta 2 agonists, asthma controller, slow onset/long acting (SOLA) |
|
|
Term
| Formoterol mode of action, use, onset/offset |
|
Definition
| beta 2 agonist; asthma controller OR reliever; rapid onset/long acting (ROLA) |
|
|
Term
| beta 1 receptor agonist PD, effect |
|
Definition
|
|
Term
| dobutamine mode of action, effect, synthetic version of? |
|
Definition
| pseudo beta 1 agonist (alpha 1 agonist and antagonism of racemic mix cancel); inotropic used by surgeons; synthetic catecholamine |
|
|
Term
| dopamine dose effects: low, medium, high? |
|
Definition
| Low (D1) = renal dose, dilates renal vasculature, increased RPF/perfusion; medium (beta 1) = heart dose, increased heart rate; high (alpha 1) = increased vasoconstriction, afterload and oxygen consumption. |
|
|
Term
| dopexamine mode of action, effect, use, synthetic version of? |
|
Definition
| D1 and beta 2 agonists at low dose, decreases afterload (vasodilation) and O2 consumption, inotropic; synthetic catecholamine (dopamine) |
|
|
Term
| fenoldopam mode of action, use, equivalent to? |
|
Definition
| selective D1 agonist; anti-hypertensive; like low dose dopamine (renal dose) |
|
|
Term
| Isoprenaline mode of action, effect, synthetic version of? |
|
Definition
| non-selective beta agonist; inotropic and vasodilation/decrease afterload (increase in O2 consumption more moderate like PDE III inhibitors); synthetic catecholamine |
|
|
Term
|
Definition
| Intrinsic sympathomimetic activity; less likely to overdose on beta blockers with this (blockers also partial agonists), no increase in TG, LDL or glucose |
|
|
Term
| selective beta 1 blockers effect, at high doses,examples? |
|
Definition
| slow heart without vascular effect; lose selectivity at high doses; metaprolol, atenolol, acebutolol |
|
|
Term
| Beta blocker effect, side effects? for overdose? |
|
Definition
| vasodilation; loss of ability to vasodilate (bad for asthma and COPD), increased TG, LDL and glucose (like diuretics), dreams if fat soluble (ex: diuretic propranolol); use inotropic insulin or glucagon for overdose |
|
|
Term
| propranolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| non-selective beta and Na channel blocker; fat soluble (dreams); Hepatatic 1A and 2D6; no ISA |
|
|
Term
| pindolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| non-selective beta and (membrane stabilizing) Na channel blocker, 5HT1a agonist; water soluble; renal excretion; strong ISA |
|
|
Term
| metoprolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| selective beta 1 blocker; fat soluble (dreams); hepatic 2D6; no ISA |
|
|
Term
| atenolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| selective beta 1 blocker; water soluble; renal elimination; no ISA |
|
|
Term
| acebutolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| selective beta 1 and membrane stabilizing Na channel blocker; fat soluble; renal elimination; ISA (also less effect on metabolic profile TG, LDL) |
|
|
Term
| nadolol mode of action, solubility?, metabolism? ISA? |
|
Definition
| non-selective beta blocker; water soluble; renal excretion; no ISA |
|
|
Term
| Water soluble beta blockers? |
|
Definition
| PANS: pindolol, atenolol, nadolol, satalol |
|
|
Term
| esmolol mode of action, delivery?, metabolism? half life? |
|
Definition
| beta blocker; IV, plasma esterases; ultra short acting |
|
|
Term
| beta blockers affect on cardio depolarization |
|
Definition
| Mainly flattens phase 4 (harder to depolarize) |
|
|
Term
| labetalol mode of action, effect, |
|
Definition
| mixed: non-cardio selective alpha/beta blocker and more; mainly reduces afterload and bronchoconstriction (alpha blocker) |
|
|
Term
| carvedilol mode of action, effect |
|
Definition
| mixed non-cardioselective alpha/beta blocker; stops vasculature from contracting (alpha blocker) |
|
|
Term
| Nebivolol mode of action, metabolism |
|
Definition
| beta blocker with NO (an EDRF) potentiating effect; metabolism by 2D6 to active moieties. NOTE EDRF = endothelium derived relaxing factor |
|
|
Term
| For beta blocker overdose? |
|
Definition
| Use inotrope insulin or glucagon (can't use beta agonist because receptor blocked) |
|
|
