Final Exam: NR567/ NR 567 (Latest 2024/ 2025 Update) Advanced Pharmacology for the AGACNP Review| Questions and Verified Answers| 100% Correct – Chamberlain
Final Exam: NR567/ NR 567 (Latest 2024/
2025 Update) Advanced Pharmacology for
the AGACNP Review| Questions and
Verified Answers| 100% Correct –
Chamberlain
Q: Direct oral anticoagulants (DOAC)
Oral Xa inhibitors
Answer:
Rivaroxaban (Xarelto) Apixaban (Eliquis)
Edoxaban (Savaysa) Betrixaban (Bevyxxa)
Q: DOAC MOA
Answer:
Inhibits factor Xain the final common pathway of clotting
Q: DOAC monitoring
Answer:
none
Q: DOAC dosing
Answer:
Rapid onset of action, shorter half-life than warfarin.
Q: DOAC indications
Answer:
1-Embolic stroke in patients with a fib without valvular heart disease
2-prevention of VTE following hip or knee surgery
3-treatment of VTE disease
Q: Reversal of anti-Xa DOAC
Answer:
Andexanet alfa
- a factor Xa “decoy” molecule without procoagulant activity that competes for binding to antiXa drugs
-Low dose 400mg IV @ 30 mg/min, then 4 mg/min for 120 min - ** Thrombotic complications have been reported, as well as cardiac arrest and sudden death.
This may only be considered as an alternate approach to life-saving bleeding on anti-Xa drugs.**
Q: Direct Thrombin Inhibitors (DTIs)
Answer:
Arbatroban & melagatroban : small mole- cules that only bind at the thrombin active site
Hirudin & bivalirudin: large, bivalent DTIs that bind at the catalytic or active site of thrombin as
well as the substrate recognition site.
Dabigatran (Pradaxa) (P.O.)
Q: Direct Thrombin Inhibitors MOA
Answer:
Directly binds to the active site of thrombin, thereby inhibiting, thrombus downstream affects.
This is in contrast to the indirect thrombin inhibitors, such as heparin and low molecular weight
heparin, which acts through antithrombin.
Q: Argatroban (DTI) indication and monitoring
Answer:
FDA approved for use in patients with HIT with or without thrombosis and coronary angioplasty
in patients with HIT
Monitoring by aPTT
Dose reduction required for liver disease
Will raise INR as well, making bridging to warfarin tricky
Q: Warfarin MOA
Answer:
Inhibits, vitamin K, dependent, coagulation, factor synthesis ->
inhibits factors II, VII, IX, and X
Q: Dabigatran (Pradaxa)
Answer:
Oral anticoagulant. Prevents thrombus formation by di- rectly inhibiting thrombin formation.
Reduces the risk of stroke and embolism for clients with nonvalvular atrial fibrillation.
Side effects: bleeding, GI discomfort
Q: Dabigatran reversal agent
Answer:
Idarucizumab (Praxbind)
Q: Fibrinolytics/Thrombolytics
Answer:
Streptokinase
Tenectoplase Reteplase Alteplase
Q: Thrombolytic MOA
Answer:
Activate plasminogen and convert it to plasmin, which digest fibrin
Rapidly lysed thrombi by catalyzing the formation of the serine protease plasmin from its
precursor plasminogen. These drugs create a generalized lytic state when administered
intravenously.
Q: Fibrinolytics/Thrombolytics indications
Answer:
Fibrinolytics:
1-PE with hemodynamic instability
2-Severe DVT , such as the superior vena cava syndrome
3-Ascending thrombophlebitis of the iliofemoral vein with severe lower extremity edema
Thrombolytics:
1-acute MI
2-ischemic CVA
Q: Aspirin MOA
Answer:
Inhibits the synthesis of the prostaglandin thromboxane A2 by irreversible acetylation of the
enzyme cyclooxygenase.
(Thromboxane A2 is what causes platelets to change shape in aggregate.)
Q: Aspirin indications for use
Answer:
The FDA concluded the aspirin is for primary prophylaxis
Q: Thienopyridines
P2Y12 Antiplatelet agents
Answer:
Clopidogrel (Plavix) Ticlopidine (Ticlid)
Prasugrel (Effient) Ticagrelor (Brilinta)
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Warfarin therapeutic dosing -Initiate with standard dosing 5-10 mg-initial adjustment of prothrombin time takes ~ 1 wk…. Usually results in maintenance dose 5-7 mg/ day.
Therapeutic range of warfarin 2-3 (INR) FOR MOST INDICATIONS, use higher range (2.5-3.5) with mechanical mitral valves
Occasionally patients exhibit warfarin resistance defined as… …. Progression or recurrence of a thrombotic event, while in the therapeutic range of warfarin.may necessitate an increase in INR range or a switch to sq LMW heparin Heparin Anticoagulant Heparin MOA Binds to antithrombin and accelerates the inhibition of clotting factor proteases IIa, IXa, and Xa. Catalyzes the inactivation of thrombin and other clotting factors. Low molecular weight heparins EnoxaparinDalteparinTinzaparin High-molecular-weight fractions of heparin Inhibit all three clotting factors- especially thrombin and factor Xa LMW effect on clotting factors Inhibit activated factor X, but have less effect on thrombin than the high molecular weight species Unfractionated Heparin Heparin Comparison of LMWH and UFH Equal efficacy, increase bio availability from subcutaneous side of injection and less frequent dosing requirements (LMWH). Heparin Indications • prevention and treatment of Venus thromboembolic disease• arterial• Prevention of thrombosis in arterial or cardiac surgery monitoring heparin therapy UFH – aPTT or PTT —————— is superior to warfarin and preventing recurrent venous thromboembolism in patients with cancer —LMWH— Warfarin in pregnant women “-Warfarin is category “”X””-The risks to the fetus are too high, and thus this medication is contraindicated in pregnancy-crosses the placenta readily and can cause a hemorrhaging disorder in the fetus or cause a serious birth defect characterized by abnormal bone formation.” reversal agent for heparin protamine sulfate Reversal agent for warfarin Vitamin K (phytonadione) Direct oral anticoagulants (DOAC)Oral Xa inhibitors Rivaroxaban (Xarelto)Apixaban (Eliquis)Edoxaban (Savaysa)Betrixaban (Bevyxxa) DOAC MOA Inhibits factor Xain the final common pathway of clotting DOAC monitoring none DOAC dosing Rapid onset of action, shorter half-life than warfarin. DOAC indications 1-Embolic stroke in patients with a fib without valvular heart disease2-prevention of VTE following hip or knee surgery3-treatment of VTE disease Reversal of anti-Xa DOAC “Andexanet alfa – a factor Xa “”decoy”” molecule without procoagulant activity that competes for binding to anti-Xa drugs -Low dose 400mg IV @ 30 mg/min, then 4 mg/min for 120 min- ” Direct Thrombin Inhibitors (DTIs) Arbatroban & melagatroban : small molecules that only bind at the thrombin active siteHirudin & bivalirudin: large, bivalent DTIs that bind at the catalytic or active site of thrombin as well as the substrate recognition site. Dabigatran (Pradaxa) (P.O.) Direct Thrombin Inhibitors MOA Directly binds to the active site of thrombin, thereby inhibiting, thrombus downstream affects. This is in contrast to the indirect thrombin inhibitors, such as heparin and low molecular weight heparin, which acts through antithrombin. Argatroban (DTI) indication and monitoring FDA approved for use in patients with HIT with or without thrombosis and coronary angioplasty in patients with HITMonitoring by aPTTDose reduction required for liver diseaseWill raise INR as well, making bridging to warfarin tricky Warfarin MOA Inhibits, vitamin K, dependent, coagulation, factor synthesis -> inhibits factors II, VII, IX, and X Dabigatran (Pradaxa) Oral anticoagulant. Prevents thrombus formation by directly inhibiting thrombin formation. Reduces the risk of stroke and embolism for clients with nonvalvular atrial fibrillation. Side effects: bleeding, GI discomfort Dabigatran reversal agent Idarucizumab (Praxbind) Fibrinolytics/Thrombolytics StreptokinaseTenectoplase ReteplaseAlteplase Thrombolytic MOA Activate plasminogen and convert it to plasmin, which digest fibrinRapidly lysed thrombi by catalyzing the formation of the serine protease plasmin from its precursor plasminogen. These drugs create a generalized lytic state when administered intravenously. Fibrinolytics/Thrombolytics indications Fibrinolytics:1-PE with hemodynamic instability2-Severe DVT , such as the superior vena cava syndrome 3-Ascending thrombophlebitis of the iliofemoral vein with severe lower extremity edema Thrombolytics: 1-acute MI2-ischemic CVA Aspirin MOA Inhibits the synthesis of the prostaglandin thromboxane A2 by irreversible acetylation of the enzyme cyclooxygenase. (Thromboxane A2 is what causes platelets to change shape in aggregate.) Aspirin indications for use The FDA concluded the aspirin is for primary prophylaxis ThienopyridinesP2Y12 Antiplatelet agents Clopidogrel (Plavix)Ticlopidine (Ticlid)Prasugrel (Effient)Ticagrelor (Brilinta) Thienopyridines MOA -Reduce platelet aggregation by inhibiting the a DP pathway of platelets.-Irreversibly block the ADP P2Y12 receptor on platelets. -these drugs have no effect on prostaglandin metabolism Ticlopidine (Ticlid) indication Approved for prevention of stroke in patients with a history TIA or thrombotic stroke, and in combo with aspirin for prevention of coronary stent thrombosis Clopodogrel (plavix) and prasugrel (Effient) indication for use Approved for patients with unstable angina or NSTEMI in combination with aspirin; recent MI, stroke, or established PAD Cangrelor (Kengreal) an IV P2Y12 inhibitor that is used as an adjunct agent for PCI for patients without previous ADP P2Y 12 inhibitor therapy Dipyridamole Vasodilator that also inhibits platelet function by inhibiting adenosine uptake in the cGMP phosphodiesterase activity. By itself it has little or no beneficial effect so therapeutic use of this agent is primarily in combination with aspirin to prevent CVA’s.Can also be used in combination with warfarin for primary prophylaxis of thromboembolism in patients with prosthetic heart valves Cilostazol (Pletal) Phosphodiesterase inhibitor that promotes vasodilation and inhibition of platelet aggregation. Used primarily to treat intermittent claudication. Platelet GB IIb/IIIa inhibitor EptifibatideTirofiban Platelet GB IIb/IIIa inhibitor MOA Reversibly binds to platelet glycoprotein IIb/IIIa receptors, reducing platelet aggregation Starling’s Law The more the heart is filled during diastole the more forcefully it contractsMore EDV = More pre-load= More SV= More forceful contraction during systole Flumazenil (Romazicon) Benzodiazepine antagonistWorks on benzodiazepina but not sedative-hypnotics, ethanol, opioids, or general anesthetics Flumazenil MOA competitive antagonist at GABA receptor Adverse effects of flumazenil Agitation, confusion, dizziness, nauseaMay cause a severe precipitated absence syndrome in patients who developed a psychological benzodiazepine dependence. And patients who have ingested benzodiazepines with tricyclic and depressants, seizures and cardiac arrhythmias, may follow administration. Loop diuretic examples furosemide, bumetanide, torsemide, ethacrynic acid Loop diuretics MOA Inhibition of the Na+/K+/2Cl transporter in the ascending limb of loop of Henle Loop diuretic indications Acute pulmonary edemaEdematous conditionsHyperkalemiaHypercalcemiaARFAnion overdose (toxic ingestion of bromide, fluoride, and/or iodide, which are reabsorbed in the TAL). Loop diuretic side effects 1-Hypokalemic metabolic alkalosis (give K supplements)2-Ototoxicity: hearing loss in renal insufficiency pts or when combined with aminoglycosides (dose related and usually reversible)3-Hyperuricemia: volume loss can precipitate gout attacks (prevented by lowering doses)4-Hypomagnesemia (PO mag)5- allergic Rx to sulfonamides (all are sulfonamides except ethacrynic acid Loop and thiazide diuretics contraindications allergy, hepatic coma, severe electrolyte lossCaution in overzealous use of any diuretic with borderline renal failure or heart failure Thiazide diuretic examples hydrochlorothiazide (HCTZ)chlorothiazidemetolazone Thiazide diuretics MOA Inhibit NaCl reabsorption from the liminal side of epithelial cells in the distal convoluted tubules by blocking the Na+/Cl transporter Thiazide diuretic indication for use HTNHeart failureNephrolithiasis d/t idiopathic hypercalciuriaNephrogenic diabetes insipidus Thiazide diuretic side effects •Hypokalemia (metabolic alkalosis)•Hyponatremia•Hypomagnesemia•hyperglycemia (impaired glucose tolerance)•Hyperlipidemia•Hyperuricemia• Potassium-sparing diuretic examples SpironolactoneAmiloride Potassium sparing diuretics MOA Reduce Na+ absorption in the collecting tubules and ducts. (Sodium absorption and potassium secretion regulated by aldosterone) Potassium-sparing diuretic side effects 1-Hyperkalemia2-Hyperchloremic metabolic acidosis: d/t inhibition of H+ secretion in parallel with K+ secretion3- Gynecomastia4-ARF (when combing with triamterene and indomethacin)5-triamterene: kidney stones Potassium-sparing diuretics contraindications HyperkalemiaChronic renal insufficiency Concurrent use of CYP3A4 inhibitors (Erythromycin, fluconazole, diltiazem, grapefruit juice) Potassium-sparing diuretic indication •Hyperaldosteronism dt any cause•Hypokalemia dt other diuretics •post-myocardial infarction Medication indicated to prevent cerebral vasospasms Nicardipine Glucagon Indications •Hypoglycemia•Beta blocker overdose•Endoscopic retrograde, cholangiopancreatography procedure to facilitate relaxation of the sphincter of Oddi drug dependence Defined as a characteristic withdrawal or abstinence syndrome, when a drug is stopped, or an antagonist is administered. drug abuse Drugs used in ways that are not medically approved, usually because they close strong feelings of euphoria or alter perception drug misuse Taken outside of a prescriptive guidelines (larger amounts over a longer time)Take him without prescription (often obtained from a friend or relative) drug tolerance Due to chronic exposure to addictive drugs, the brain shows signs of adaptation. Medications for alcohol abuse Naltrexone (ReVia)Acamprosate (Campral) Disulfiram (Antabuse)Topiramate (Topamax) Naltrexone (ReVia) -Initial treatment for alcohol use disorder-Started while still drinking-Can treat concurrent opioid use disorder-Contraindicated in liver disease-Maybe given monthly in long acting injections Acamprosate (Campral) -treats alcohol withdrawal symptoms-Must abstain from alcohol prior to beginning treatment Disulfiram (Antabuse) -Blocks oxidation of alcohol-Abstain from alcohol prior to treatment to avoid a reaction-Medication alone has a little effect, but flushing, throbbing, headache, nausea, vomiting, sweating, hypotension, and confusion occur within a few minutes after an individual taking this medication drinks alcohol and may last 30 minutes in mild cases, or several hours in severe ones. Topamax for ETOH -blocks sodium channels and enhances GABA-A-Reduces cravings for alcohol Medications/Plan for the treatment of alcohol withdrawal syndrome Substitute a long-acting sedative-hypnotic (benzos) drug for alcohol, and then gradually reduce or taper the dose of the long acting drugLong-active benzos: chlorodiazepoxide (Librium) & diazepam (Valium) (not for pts with liver disease) Short-acting: lorazepam (Ativan) & oxazepam (Serax)Electrolyte balancing: k+, mg, phosIV thiamine/B1: protect against wernicke-korsakoff syndrome Hypoglycemic mgmt w/ glucose Local anesthetic medication classes Amide-linked (metabolized my liver enzymes)Ester-linked (metabolized in the plasma) Examples of ester-linked local anesthetics ProcaineCocaineTetracaineBenzocaineChloroprocaine examples of amide-linked local anesthetics LidocainePrilocaineEtidocaineMepivacaineBupivacaineRopivacaineArticaineDibucaine What happens when you add epinephrine to a local anesthetic such as lidocaine? Extends the duration of the anesthesia block- making it useful for a longer procedure. Shortens time to achieve anesthetic effect. MOA of local anesthetics Blockade of voltage-gated sodium channelsAnd when progressively increasing concentrations of a local anesthetic are applied to a nerve fiber, the threshold for exultation increases, impulse conduction, slows, the rate of rise of the action, potential declines, action, potential, amplitude, decreases, and the ability to generate an action potential is completely abolished. This is the results from binding of the local anesthetic to more and more sodium channels. Bupivacaine indications Short term infusions only (bc of cardiotoxicity):-spinal anesthetic for epidural infusion for postop pain control (because of its longer duration of action) and for labor analgesia-digital block Procaine indications dental anestheticcompared to lidocaine, it has poor penetrating ability and little systemic toxicity. Shorter duration of action – up to 1.5 hrs. Lidocaine (local anesthetic) indications Spinal, epidural, IV, topical administration Major and min peripheral blocks contraindications in local anesthetics no added episodes for digital blocks or areas that lack collateral circulation Adverse effects associated with medications to treat psychosis pseudodepression, akinesia, toxic confusional statesextrapyramidal reactions: parkinsonian syndrome, akathisia (uncontrollable restlessness), acute dystonic reactions (spasmodic retrocollis or torticollis)Tardive dyskinesiaProlonged QTSeizuresagranulocytosis (clozapine)Neuroleptic Malignant Syndrome Neuroleptic Malignant Syndrome (NMS) – NMS is like S & M- You get hot (hyperpyrexia)- stiff (increased muscle tone)- Sweaty (diaphoresis)- BP, pulse and resp go up – Start to droolelevated CK, leukocytosis, treat: Benadryl, cooling, benzos positive inotropic agents definition drugs that stimulate the heart to increase the force of contractions Examples of positive inotropic agents digoxin (cardiac glycoside)milrinone (bipyridine)Dobutamine (selective beta1 agonist)Dopamine Chronotropic drugs drugs that influence the rate of the heartbeat Alpha-1 adrenergic receptors constricts blood vesselsconstricts bladder neck Beta-1 adrenergic receptors increased HR & contractilityincrease renin Beta-2 adrenergic receptors increased glucosedecrease peristalsisrelaxes uterusdilate bronchi Treatment for hypovolemic shock fluids, blood, vasopressors Levophed (norepinephrine) Epinephrine ~Nonspecific adrenergic agonist~First-line treatment for allergic reactions and anaphylaxis~Other uses: hypovolemic, distributive shock~Off-label uses: acute severe asthma that is unresponsive to inhaled beta-agonist, asystole/pulseless arrest, pulseless ventricular tachycardia, ventricular fibrillation, bradycardia that is unresponsive to atropine or pacing, inotropic support. Phenylephrine (Neo-Synephrine) Dopamine Dobutamine (Dobutrex) activation of the sympathetic nervous system caused by what drugs sympathomimetics – activate fight or flight and affect SVR and CO causes of obstructive shock cardiac tamponade, tension pneumothorax, pulmonary embolism treatment of obstructive shock mechanical decompression, anticoagulants/fibrolytics, surgical decompression distributive shock anaphylaxis, sepsis Treatment of distributive shock pressors and fluids cardiogenic shock MI, cardiac valve disease, dysrhythmia treatment for cardiogenic shock inotropes, vasoconstrictors Angiotensin-converting enzyme (ACE) inhibitors MOA antihypertensive drug blocks the conversion of angiotensin I to angiotensin II, and inactivates bradykinin – causing blood vessels to relax and dilate (decreased peripheral vascular resistance). ACEi indications for use HTNHFpost MIDM Renal failure (diminish proteinuria & stabilize renal function) Contraindications of ACEi pregnancy d/t fetal harmbilateral renal artery stenosis ACEi side effectsRemember A-C-E Mnemonic “hyperkalemia (“”E”” for electrolyte)dry cough (“”C”” for cough)angioedema (“”A””)wheezing (sometimes)ARF in pts with vital renal stenosis” ACEi examples CaptoprilEnalaprilLisinoprilRamipril Angiotension receptor-blocking (ARBs) agents MOA selectively blocks (antagonizes) angiotensin II, which decreases PVR, increases Na+ and water release, and K retention. ARB examples LosartanValsartanCandesartan ARB indications for use HFCKDfor pts who had adverse rx to ACEi ARB contraindications pregnancy, bilateral renal artery stenosis ARB adverse effects -Hyperkalemia-Hypotension-Acute renal failure in pts with bilateral renal artery stenosis-Rash, fever, altered taste-No cough-Lower angioedema risk Vasodilator examples hydralazineminoxidilnitroprusside Calcium channel blockers (CCBs) MOA Reduction of peripheral resistance and blood pressure via inhibition of calcium influx into arterial smooth muscle cells.Anti-arrhythmic and antianginal effects. CCB examples diltiazemamlodipinenicardipinenifedipine CCB side effects flushingdizzinessnauseaconstipationperipheral edemaToxicities: bradycardia, AV block, cardiac arrest, heart failure CCB uses anginaHTNSVThypertrophia cardiomyopathymigrainesRaynauds phenomenon Beta Blockers MOA Blocks the beta-adrenergic receptors in heart; decreases excitability of heart, reduces cardiac workload and oxygen consumptionPropanol – nonselective B blockadeMetoprolol & atenolol – cardioselective B1 blockadeNadolol & Carteolol – nonselective B blockageLabetolol, Carvedilol & Nebivolol – 3:1 ratio of B:a antagonism. beta blocker contraindications Asthma – propranolol Block (heart block), bradycardia – propranololDiabetes – propanolol BB indications Propanolol – HTN, reflex tachycardia d/t direct vasodilators, post MI, HFMetoprolol & Atenol – HTN in ppl w/ asthma, DM, PVDNadolol & Carteolol – HTN, anginaLabetolol, Carvedilol, & Nebivolol – HTN & HF, HTN of pheochromocytoma, HTN emergency Short acting Insulins Long Acting Insulins NPH (Novolin N; Human N)Insulin glargine (Lantus)Insulin determir (Levemir) Insulin deluded (Tresiba) Type of insulin used for an IV insulin drip and indication regular insulin DKA or periop mgmt of glucose Rapid insulin – Onset, peak, duration Onset: 5-15 minPeak: 1-1.5 hrDuration: 3-4 hr Regular insulin – Onset, peak, duration Onset: 30-60 minPeak: 2 hrsDuration: 6-8 hr NPH – Onset, peak, duration Onset: 2-4 hrPeak: 6-7 hrDuration: 10-20 hr Insulin glargine and detemir – Onset, peak, duration Insulin degludec – Onset, peak, duration Onset: 0.5 – 1.5 hrPeak: noneDuration: >42 hr Insulin mechanism of action Metabolic action is ANABOLIC.Promotes energy conservation and storage of glycogen, cell growth and division, transport of glucose, amino acids, nucleotides, and potassium. *Stimulates the synthesis of complex organic molecules.
GLP-1 glucagon-like peptide 1
TZD Thiazolidinedione
DPP4-I/ DPP-4i dipeptydl peptidase – 4 inhibitors
SGLT2i sodium-glucose cotransporter 2 inhibitor
Drug class to be considered for diabetes management prior to insulin GLP-1s
Sulfonylureas MOA
Examples of sulfonylureas glyburideglipizideglimepiride
Biguanides Metformin (Glucophage)
Biguanide MOA Decrease hepatic glucose production and intestinal glucose absorption; increase insulin sensitivity
Biguadine side effects, special considerations, and Contraindication GI upset – anorexia, nausea, vomiting, abdominal discomfort, diarrhea (helps to med with food). Can be given to pt with GFR 45-60start this med at diagnosis of DM2Can cause lactic acidosis on renal insufficiencyCONTRAINDICATED FOR GFR LESS THAN 30
TZD MOA Reduces glucose levels by decreasing insulin resistance.Works on muscle, adipose tissue, and the liver. Increased uptake in the tissues. Piogltazone lowers triglycerides and raises HDL
TZD examples Pioglitazone (Actos)Rosiglitazone (Avandia)
TZD side effects and contraindications
GLP-1 examples Exenatide (Byetta)Liraglutide (Victoza)Dulaglutide (Trulicity)Semaglutide (Ozempic)
GLP-1 MOA activates receptors for GLP-1, causing the same effects of endogenous incretins – slowing gastric emptying, stimulating glucose-dependent insulin release, inhibiting glucagon post prandial release, and suppressing appetite
GLP-1 side effects and contraindications Weight loss (think Ozempic!)N/V/DIncreased risk of pancreatitisContraindicated in pts with PMx or Family Hx of Medullary thyroid CA or Multiple endocrine neoplasia (MEN) type 2
DM2 med classes that work by binding to the sulfonylurea receptor and stimulate insulin secretion SulfonylureasmeglitinidesD-phenylalanine derivatives
DM2 med agents that lower glucose levels by their actions on liver, muscle, and adipose tissue BiguanidesTZDs
DM2 agents that principally slow the intestinal absorption of glucose alpha-glucosidase inhibitors
DM2 agents that mimic incretin effect or prolong incretin action GLP-1 receptor agonistsDPP-4 (dipeptidyl peptidase 4) inhibitors
DM2 agents that inhibit the reabsorption of glucose in the kidney SGLTs
DM2 agents that act by other or ill defined mechanisms pramlintidebromocriptinecolesevelam
SGLT2 inhibitors MOA *filtration and prevents reabsorption of glucose in the renal tubulesIncreased glucose secretion via urine, which lowers glucose levelswt loss dt caloric loss via urine
SGLTi side effects/contraindications Volume depletion and hypotensionUTIGenital mycotic infectionsPyelonephritissepticemiaFourniers gangrene*Reduced efficacy in pts with CKDNot recommended for GFR <45CONTRAINDICATED for GFR <30 & DM1 and DM2 w/ insulin deficiency DPP4-i MOA enhances incretin hormones’ actions, stimulating glucose-dependent insulin release and suppressing the postprandial release of glucagon. Increased insulin release and reduced glucagon release. Decreased hepatic glucose production. DPP4-i side effects/contraindications predisposition to nasopharyngitis and URIs D-Phenylalanine Derivative MOA stimulates rapid and transient release of insulin from beta cells thru closure of the ATP-sensitive K+ channel D-Phenylalanine Derivative Side effect hypoglycemia example of D-phenylalanine derivative Nateglinide (Starlix) afterload the resistance against which the heart must overcome to pump blood out through aorta (overcome SVR). Classes of drugs that decrease afterload Beta blockersCCBVasodilators preload degree of stretch of the cardiac muscle fibers at the end of diastole, prior to contraction Drugs that increase afterload Vasopressors drugs that decrease preload diureticsnitratesACEi/ARBsCCB (Mild) What increased preload volume/IVF/Blood product Digoxin (Lanoxin) cardiac glycoside that inhibits the Na+/K+-ATPase (sodium pump) giving it positive inotrope properties. Increases cardiac contractilityincreases cardiac outputslows HR (negative dromptropic)toxicity is worsened by hypokalemiahyperkalemia diminishes this meds effectstoxic effects:heart blocks, arrhythmias, tachycardia, cardiac arrest Negative dromotropic meds Slow cardiac conductioncardiac glycosides CCBBB Positive dromotropic drugs accelerate cardiac conductionEpinephrinedopaminedobutamine preferred anti-seizure medication for a generalized seizure disorder in a pregnant female Levetiracetam (Keppra) or lamotrigine (Lamictal) Antipsychotic medication that can cause acute dystonia after early initiation Haloperidol (Haldol) Dystonia a condition of abnormal muscle tone that causes the impairment of voluntary muscle movement Long acting benzo used to treat anxiety diazepam (Valium) Alternate uses of antiseizure medications teratogenic anti seizure medications valproate (Spina bifida; cognitive impairment/ spectrum disorder)phenobarbital (congenital malformations/cardiac defects)topiramate (oral clefts – esp in first trimester) Broad spectrum antiseizure meds ValproateLevetiracetamTopiramateZonisamideRufinamide Sodium channel blocker antiseizure meds CarbamazepineOxcarbazepineLamotrigineLacosamidePhenytoin/Fosphenytoin Barbiturate Antiseizure meds phenobarbital primidone gabapentinoid antiseizure meds gabapentinpregabalin absent seizure specific med ethosuximide Benzos for seizures diazepamclonazepamclobazam Benzos for status epilepticus lorazepam and midazolam Insulin infusion given for DKARegular insulin starting at 0.1 units/kg/hr DKA treatment Fluid therapy beginning with NSstart Regular insulin drip 0.1 u/kg/hr and titrate per q1hr finger stickNa+, K+ lyte replacementPt with likely be acidotic, pH less than 7.3, Kussmauling, N/V, ketonuria, glucusuria HHS treatment -Agressive rehydration w/ IVF-restoration of glucose and electrolyte homeostasis -may need low dose insulin-Pt will have super high plasma glucose but lack ketones/acidosis. Nitrates for angina Vasodilator/antiangina vasodilator effect on the peripheral arteries and veinsReduces cardiac O2 demand, decreasing preload, dilating coronary arteries, improving collateral flow, and reducing afterloadRoutesSublingual: every 5 minutes x 3 doses; if no relief, consider IV nitroglycerinIV: indicated for persistent ischemia or concurrent hypertension or heart failureCaution: patients who have taken sildenafil or another phosphodiesterase inhibitor within 24 hours should not receive nitratesCaution: nitrates cause hypotension Antithrombotics in ACS Morphine in ACS mild vasodilation, provides pain relief Statin in ACS admin ASAP then daily Oxygen in ACS O2 sat <90% or for those who have respiratory distress or signs of hypoxemia BB for ACS anti platelet for ACS/MI Give ASA/PlavixLoading dose for ASA (NSTEMI) – 162-325 mg non-enteric coated PO ASAP (chewed or crushed), then 75-100 mg daily. Loading dose for Plavix (NSTEMI/STEMI) – 600 mg PO STAT then 75 mg daily for at least 1 year. ACEi/ARB post MI -Reduces cardiac remodeling post-MI-Continue daily dose indefinitely-Improves patient survival in those with heart failure or anterior myocardial infarction-Administer to patients with hypertension, diabetes, or chronic kidney disease (CKD) unless contraindicated thrombolytic agents reteplasealteplasetenecteplase Contraindications to thrombolytics ~history of recent stroke~history of recent intracranial or intraspinal surgery~history of recent serious head trauma~intracranial neoplasm, aneurysm, or arteriovenous malformation~known bleeding disorder~severe uncontrolled hypertension Fibrolynic agents should be given within ___ hours of onset of symptoms 2 hours Hypertensive crisis >180 / >120with signs or symptoms of acute ongoing end target-organ damage, such as acute pulmonary edema, hypertensive encephalopathy, aortic dissection, myocardial infarction, stroke, or blindness.
sedative means anxiolytic
hypnotic means produces a state of drowsiness and encourages the onset and maintenance of a state of sleep more pronounced depression of CNS
sedative-hypnotics Benzosbarbituatesnewer hypnotics melatonin receptor agonistsorexin antagonists5-H2-Receptor agonists
Benzo MOA & indications and cautions and s/e bind to GABAa receptor subunits at CNS neuronal synapses facilitating GABA-mediated chloride ion channel opening frequency -> enhances membrane hyperpolarizationFor anxiety, panic attacks, anesthesia adjunct (skeletal muscle relaxant), seizures, insomniadon’t combine with CYP450s
Barbiturate MOA, examples, indication bind to GABAa receptor subunits at CNS neuronal synapses facilitating GABA-mediated chloride ion channel opening durationEx: Phenobarbital, pentobarbitalseizures (pheno), anesthesia (thio), insomnia (seco)
Newer hypnotic MOA, examples, indication, contraindication bind selectively to subgroup of GABAa receptors, acting like benzodiazepines to enhance membrane hyperpolarizationEx: Zolpidem (Ambient), eszopiclone (Lunesta), zaleplon (Sonata)FOR: sleep disordercaution in liver disease, avoid alcohol, half
melatonin receptor agonist MOA and example activates MT1 and MT2 receptors in the subchiasmatic nuclei in the CNS. Half-life prolonged by CYP3A4s.EX: Ramelton (Rozerem)
5-HT-Receptor Agonist MOA and example, side effects Mechanism uncertain: partial agonist at 5-HT receptors but affinity for D2 receptors also possibleEx: BuspironeNonspecific CP, tachycardia, dizziness, paresthesias, increased BP when combined with MAOIs, constricted pupils
phenothiazines MOA, examples, use, Side effects
Haloperidol MOA Blockade of D2 receptors>> 5H2A receptorsUse: Schizophrenia’s positive symptoms, bipolar (manic), Huntington chorea, Tourettes syndrome QT prolonged, EP side effects
Second gen antipsychotics aripiprazole (Abilify), Brexpiprazole (Rexulti), cariprazine (Vryalar), clozapine (Clozaril), lurasidone (Latuda), olanzapine (Zyprexa), quetiapine (Seroquel), risperidone (Risperdal), ziprasidone (Geodon)MOA: blockade of 5-H2a receptors > blockade of d2 receptorsS/E: clozapine: agranulocytosis ziprasidone: QT prolong cloz & olaz: DM & wt gain ~~ risperidone: hyperprolactinemia (give bromcriptine).
Lithium
Indications for NMBAs RSIreduce shivering during TTMoptimize mechanical ventilationsurgeryincreased ICPEarly ARDS to improve oxygenation
Depolarizing NMBA Succinylcholine (Anectine)
Succynylcholine (Anectine)
malignant hyperthermia A hereditary condition of uncontrolled heat production that occurs when susceptible people receive certain anesthetic drugs.muscle rigidityhyperthermiarapid onset tachycardia and hypercapniahyperkalemiametabolic acidosisoften related to succinylcholine
treatment for MH Dantrolene (to reduce Ca+ release from the sarcoplasmic reticulum)cooling measures, electrolyte correction, acid-base balance correction
Etomidate (Amidate) *for RSI (especially for pts with reduced cardiac contractility) hypnotic but not analgesic propertiesNO CONTINUOUS INFUSION BC OF ENDOCRINE FX (adrenocortical suppression)S/E: potent cerebral vasoconstrictor- restricts cerebral blood flow and decreases ICP; myoclonus, no changes in CV, minimal resp fx Dexmedetomidine (Precedex) ~highly selective a2-adrenergic agonist~Hypnosis d/t stem of a2 receptor in locus coerleus~Analgesia effect from level of spinal cordHypnosis resembles physiological sleep state thru activation of endogenous sleep pathwaysS/E: mod decrease in HR, SVR, BP. can cause bradycardia, heart block, and systole from unopposed vagal stimulation. No FX on resp statusUsed for short term sedation: MV, adjunct to general anesthesia, during awake fibrotic tracheal intubation or regional anesthesia. Ketamine (Ketalar) Propofol (Diprivan) general anestheticMOA thru potentiation of the chloride current mediated through the GABAa receptor complexrecovery good without much of a hangover feelingawakening 8-10 mins after inductionHypnotic, but NO analgesic FXGeneral suppression of CNS, but may see twitching during induction. Safe to give to epileptic pts. Decreases cerebral blood flow and ICP. Lg doses produces burst suppression on EEG. S/e: hypotension, bradycardia (profound vasodilation in venous and arterial circ), asystole, potent respiratory depressant – apnea post induction; reduction of upper airway reflexes (good for intubation); propofol metabolic acidosis (propofol pH 7.0); pain on injection, Barbiturates as anesthesia dose dependent CNS depression from sedation to general anesthesia when given as bolus injectionsdo not cover analgesia – may REDUCE pain threshold, causing hyperalgesia.Potent cerebral vasoconstrictors – produce decreased cerebral blood flow, volume, and ICP. Provide neuroprotection from focal cerebral ischemia (CVA, etc). decrease electrical activity on EEG and can be used as anticonvulsantsS/E: decrease in bp d/t vasodilation, negative inotropic fx, compensatory increase in HR. Respiratory depression. IV benzos for anesthesia – side effects potent anticonvulsantstx of status epileptics, ETOH wd, local-anesthetic induced seizuresdecrease in BP (greatest with midazolam), minimal resp depression/transient apnea, disadvantage – delayed emergence Dose reduce in elderly nondepolarizing NMBAs inhibit the Ach receptor on the motor endplate, with the NMBA binding to the Ach receptor either by physically obstructing the ion channels or by preventing the conformational change in the receptor so that the endplate potential does not occur.PancuroniumRocuroniumVecuronium NMBA with least cardiovascular side effects Pancuronium IVP meds for RSI Fentanyllidocaine IV adjunctive meds toanesthesia benzosopioidslidocaineantiemeticsdexamethasone conscious sedation Administered by non-anesthesiologistsLight sedation, patient still responds to commandsMany drug options: propofol, midazolam, diazepam Thyroid storm aka thyrotoxic crisissudden and acute exacerbation of all of the symptoms of thyrotoxicosis, presenting as a life-threatening syndrome. occurs when pts with severe thyrotoxicosis undergo major surgery or develop a severe illness (such as an infection like sepsis)characterized by profound hyperthermia (105F+), sever tachycardia, restlessness, agitation, tremor.Unconsciousness, coma, hypotension, and heart failure may ensue. These symptoms are d/t excessive levels of thyroid hormones. This is life threatening if not treated immediately.
treatment for thyroid storm Potassium iodide – retards release of thyroid hormones from glandPropylthiouracil (PTU) – blocks hormone synthesisMethimazole – suppresses hormone synthesis (10x more potent than PTU, , drug of choice in adults and children)Propanolol – treat tachycardiaHydrocortisone – blocks conversion of T4 to T3 which rapidly reduces the level of thyroactive material in blood. Supportive tx: control fever with Tylenol, IVF, cooling, tx heart failure, and underlying illness that precipitated thyroid stormLast ditch: bile sequestrons (Question), plasmapheresis, PD to reduce levels of circulating thyroxine
Levothyroxine (Synthroid) ~treats hypothyroidism~Replaces thyroxineBBW- not for obesity or weight loss – larger than necessary doses may be life threatening.6-8 weeks recheck TSH
Levothyroxine interactions -Warfarin is enhanced-increased risk of catecholamine-induce arrhythmias-digoxin and insulin may require increased dosages
PTU (propylthiouracil) tx of hyperthyroidism~treatment of choice for patients in the first trimester of pregnancy~BBW- severe hepatic failure/injury, including need for transplant have occurred reserve for patients intolerant to methimozaole (other than agranulocytosis or hepatitis)S/E: hepatotoxicity, agranulocytosis, thrombocytopenia, aplastic anemia (most severe)
Methimazole for hyperthyroidism or thyroid stormCONTRAINDICATED in first trimester of pregnancyS/E: agranulocytosis, leukopenia, thrombocytopenia, aplastic anemia, hepatotoxicity, altered sense of taste and smell
Thioamides PTU & methimazole
Agranulocytosis with thioamides infrequent but potentially fatal adverse effect of either thioamide. Usually rapidly reversible when drug is discontinued. Broad spectrum abx. May need to employ colony-stimulating factors to hasten recovery
Iodides inhibit thyroid hormone release and decrease size and vascularity of hyperplastic gland should be started after thioamides because iodides they cause an increase in intraglandular stores of iodide- which delay onset of thioamide therapy or prevent use of radioactive iodide.
radioactive iodide cannot be given in pregnancy or to nursing mothers – crosses placenta/breast milk and destroys fetal thyroid gland
agranulocytosis sore throat, high fevercheck WBC, LFTs, throat cxConsider giving abx, G-CSF
Potassium iodide in prep for surgical thyroidectomyinhibits release of thyroid hormones, reduces size and vascularity of glandonset in 2-7 days