Final Flashcards
These opioid receptors are the most important pharmacologically. When stimulated they produce analgesia, euphoria, respiratory depression, and sedation. With knockout mice who didn’t have the receptor morphine was ineffective.
Mu receptors
These opioid receptors when activated produce analgesia and sedation.
Kappa receptors
These opioid receptors don’t interact with known opioids.
Delta receptors
This class of opioid drugs activate mu and kappa receptors and include morphine, codeine, meperidine, and other morphine like substances.
pure opioid agonists
This class of opioids works depending on the receptor type. They are antagonists at the mu receptor and agonists at the kappa receptor. This class includes pentazocine, nalbuphine, and butorphanol.
agonist-antagonist opioids
This opioid drug is unique because it is a partial agonist at mu receptors and an antagonist at kappa receptors.
Buprenorphine
This class of drugs act as an antagonist at mu and kappa receptors. It includes Naloxone, which is an antidote to overdose.
pure opioid antagonists
This prototype opioid used for moderate to severe pain relief. It’s actions include drowsiness, mental clouding, anxiety reduction, and a sense of well being. It acts through the CNS and the periphery and prolonged use will lead to tolerance and dependence. Adverse effects include respiratory depression, constipation, orthostatic hypotension, urinary retention, cough suppression, biliary colic, emesis, elevated ICP, euphoria/dysphoria, sedation, miosis, neurotoxicity, and with prolonged use hormonal changes and immune system alterations.
Morphine
After using opioids like morphine for a long time this develops to the effects of analgesia, euphoria, sedation, and respiratory depression. It takes increasing doses to get the same response. It also develops for oxycodone, methadone, codein, and heroin.
tolerance
This can develop in regards to morphine and other opioids and raises the abuse potential. This is the reason that opioids have to be slowly withdrawn, and if they aren’t symptoms such as yawning, rhinorrhea, sweating, sneezing, diarrhea, abdominal cramps, muscle pain/spasms, gooseflesh, and kicking.
physical dependence
What do fentanyl, alfentanil, remifentanil, meperidine, methadone, heroin, hydromorphone, oxymorphone, and levorphanolhave in common?
They are all strong opioids.
What do codeine, oxycodone, hydrocodone, and propoxyphene have in common?
They are moderate to strong opioids.
This drug crosses the BBB where it is converted to monoacetylmorphine and morphine. These two substances are responsible for the effects of this drug. It has better lipid solubility than morphine.
heroin
What are the three dosing guidelines for the clinical use of opioids?
assessment of pain - pain status should be evaluated before and 1 hour after opioid use. Dosage determination - opioid doses should be adjusted to accomodate individual variation. Dosing schedule - should be fixed q4 for best results.
This drug is the prototype opioid antagonist that is a structural analog that blocks opioid action. It can be given IM, IV, or subQ. It is used for the reversal of opioid OD, reversal of postoperative opioid effects, and the reversal of neonatal respitratory depression.
Naloxone (Narcan)
This type of headache occurs in a series and last from 15 minutes to 2 hours, and can happen two to three times a day. They are marked by unilateral pain in the inner eye.
cluster headaches
These are the most common type of headache and they tend to take on a headband distribution.
Tension headaches
This type of headache is caused by a neurovascular disorder and involves the inflammation and dilation of intracranial blood vessels.
Migraine headache
The type of migraines where there is an aura present 10-30 minutes before the actual headache where patients report flashes of light, blank areas in the field of vision, or zigzag patterns.
Migraines with aura (classic migraine)
this type of migraine makes up 70% of all migraines and has the same pain with no aura.
Migraines without aura (common migraine)
the following are symptoms for what condition: throbbing head pain, nausea, vomiting, photophobia, phonophobia, hands and feet are cold and sweaty, intolerable to odors, tinnitus, blurred vision, auras, and physical activity intensifies the pain.
Migraines
Name several triggers for migraines.
emotions (stress, anxiety, depression, excitement, frustration), foods (MSG, tyramine, phenylethylamine, yellow food coloring, aspartame), drugs (nitroglycerin, cimetidine, cocaine, alcohol, analgesics, birth control, caffeine), weather (barometric pressure changes, low/high temps), estrogen, carbon monoxide, loud noises, hypoglycemia, sleep issues.
These drugs are a first line drug to abort an ongoing migraine attack and are also known as triptans. They can be taken sub Q, intranasal, and orally and work by constricting intracranial blood vessels and suppressing the release of inflammatory neuropeptides (namely the release of calcitonin gene-related peptide (CGRP) in trigeminal pathways.) Adverse effects are usually mild but include heavy arms and chest pressure, coronary vasospasms, and a teratogenic effect demonstrated in rabbits.
Serotonin 1b/1d agonists (sumatriptan or Imitrex)
This drug is used for migraines and has a similar MOA to triptans but is well tolerated. It can also be used for cluster headaches. Adverse effects include nausea, vomiting, numbness, tingling, tachycardia or bradycardia. OD can cause “ergotism” which is all of the side effects mentioned above plus ischemia, cold extremities, and myalgia.
Ergotamine
This drug is like ergotamine, it has the same action, but less side effects.
dihyroergotamine
What is unique about these drugs: beta blockers (propanolol/inderal), calcium channel blockers (verapamil/Calan), angiotensin II receptor blocker (Candesartan), TCA’s (amitriptyline/Elavil), anticonvulsants (divalproex/Depakote and topiramate/Topomax), estrogens and supplements like vitamin b2, coenzyme Q-10, butterbur, and feverfew.
They are all drugs used for the prophylaxis of migraines.
What are the treatment options for cluster headaches?
primary therapy is prophylaxis by utilizing prednisone, lithium, or verapamil. can also be aborted with oxygen and sumtriptan.
What are the treatment options for tension headaches?
nonopioid analgesics such as acetaminophen or NSAIDS, amitryptalin (TCA), also the patient should be taught better stress management.
This progressive autoimmune inflammatory disorder targets the joints and the synovial tissue. There is often symmetric joint stiffness and pain and there can be either spontaneous remission or steady progression. Systemic manifestations include fever, weakness, fatigue, weight loss, thinning of skin, scleritis, and corneal ulcers.
rheumatoid arthritis
What are the current guidelines for the treatment of rheumatoid arthritis?
It is currently aggressive, you start with a DMARD early on to stop disease progression and give NSAIDS until the DMARD takes effect. Use glucocorticoids for flare up and short course management, and add another DMARD if the first one doesn’t work.
What did the old guidelines for rheumatoid arthritis treatment look like?
start with NSAIDS, if symptoms persist add DMARDs, and glucocorticoids may be used until DMARDS take effect.
This non biological DMARD(I) is a first choice treatment for rheumatoid arthritis. It is rapid acting and 80% of patients improve. It is a type of chemotherapy. It’s MOA is that it inhibits folic acid synthesis (specifically formation of THF) and inhibits the enzyme dihydrofolate reductase. Folic acid is needed for essential cell processes and this drug prevents immune cells from dividing. It takes 3-6 weeks for benefits to be seen. Adverse effects include hepatic fibrosis, bone marrow suppression, GI ulceration, pneumonitis, and fetal death and abnormalities.
Methotrexate (Rheumatrex)
The following drugs belong to which drug class: hydroxychloroquine (plaquenil), Minocycline (minocin), leflunomide (Arava), sulfasalazine (azulfidine).
DMARDS I
This DMARD II is a tumor necrosis factor blocker functions by binding to TNF and making it so that it can’t interact with its receptors. It costs $14K-$37K per year and is usually combined with methotrexate for treatment although it works slightly better to delay progression. It is used for moderate to severe rheumatoid arthritis, ankylosing spondylitis, plaque psoriasis, and psoriatic arthritis. Adverse effects include increased risk of infection, injection site reactions, heart failure, CNS demyelinating disorders (MS, optic neuritis), and hematologic disorders, and cancer.
Etanercept (Enbrel)
This DMARD II drug is a tumor necrosis antibody for rheumatoid arthritis and Crohn’s disease. It is used in combination with methotrexate.
Inflixamab (Remicade)
This DMARD II is a monoclonal antibody to tumor necrosis factor. It is used for moderate to severe rheumatoid arthritis and is well tolerated.
Adalimumab (Humira)
This DMARD II is an interleukin-1 receptor antagonist. It is structurally similar to a naturally occuring antagonist and superior to a placebo when it comes to symptom reduction. It is used with methotrexate.
Anakinra (Kineret)
This newer DMARD is a monoclonal antibody directed against CD20 which is an antigen on B cells. It is used more as a chemotherapeutic agent for NonHodgkin’s lymphoma.
Rituximab (Rituxan)
This newer DMARD is a T cell activation inhibitor. It was approved in 2007 and is a monoclonal antibody directed against the R in antigen presenting cells. It is a complex of cytotoxic T-lymphocyte associated antigen and Ig G1
Abatacept (Orencia)
This newer DMARD is a new TNF-alpha antibody. It was in a case study.
Simponi
This recurrent inflammatory disorder causes episodes of severe joint pain typically in the large toe. It is caused by hyperuricemia and when this becomes chronic then tophi, which are large gritty deposits in the joint form along with crystals of sodium urate. Inflammation is due to these deposits. It is essentially caused by either excessive production of uric acid or impaired renal excretion of uric acid.
gout
This antiinflammatory works by disrupting the microtubules in leukocytes and inhibiting leukocyte migration and infiltration. It is used to treat acute gout attacks, reduce incidences of attack, and abort an impending attack. Adverse effects include gastrointestinal effects (injury to rapidly proliferating cells), when used IV bone marrow suppression, renal failure, and hepatic necrosis are possible. This drug is usually reserved for unresponsive gout or patient who are intolerant of safer agents.
Colchicine
This drug blocks uric acid formation. It is used for chronic tophaceous gout and for hyperuricemia due to chemotherapy. It is well tolerated by adverse effects include hypersensitivity syndrome which is rare but potentially fatal and is marked by rash, fever, and dysfunction of the kidneys and liver. Gastrointestinal and neurological disorders (drowsiness, headache, and cataracts) are also possible.
Allopurinol (Zyloprim)
This drug for treating gout was approved in 2009 and was the first new drug in 40 years. It’s MOA is that it lowers urate levels by inhibiting xanthine oxidase. Adverse effects include abnormal liver function, abnormal arthralgia, rashed, and CV events at high doses.
Feboxustat (Uloric)
This drug for gout is the first choice for gouty arthritis. It is an NSAID with minimal GI side effects and can cause headaches as an adverse reaction.
Indomethacin (Indocin)
This drug for gout increases renal secretion of uric acid by inhibiting reabsorption. It also competes for a receptor with penicillin if they are given concurrently.
Probenacid (Benemid)
This drug for gout reduces hyperuricemia in patients with chronic gout by enhancing excretion. It is similar to probenacid.
Sulfinpyrazone (Anturane)
This is a preparation containing microbes or viruses. If it is administered it causes the immune system to manufacture antibodies.
vaccine
What is the difference between a killed or live vaccine?
killed vaccines contain whole or parts of the microbe whereas live vaccines carry live microbes that are weakened or avirulent.
This is a bacterial toxin that has been changed to a nontoxic form. It leads to antitoxins.
toxoid
This is the endogenous production of antibodies that are long lasting, it takes weeks to months to happen.
active immunity
This is conferred by giving a patient preformed antibodies and has an immediate response.
passive immunity
The administration of this provides immediate passive immunity. Concentrated antibodies are made from donated blood.
specific immune globulins
Local reactions such as discomfort, swelling, and redness, fever, anaphylaxis, acute encephalopathy, and vaccine associated paralytic poliomyelitis are all adverse effects of what process?
Immunization
This vaccine is a combination of 3 live viruses or in some instances 4 live viruses.
MMR (measles mumps rubella) or MMRV
This vaccine is bacterial in origin and consists of diptheria, a tetanus toxoid, and acellular pertussis.
DTaP
This vaccine used to be a live oral vaccine back in the day but now has been replaced by 3 inactivated serotypes for the disease (IPV, Salk vaccine )
poliomyelitis - polio virus
This vaccine has been available in Japan for a lot longer than the US. It contains the varicella-zoster virus. Can be the live attenuated virus or in combination with MMR.
Varicella (chickenpox)
This vaccine is for bacteria and meningitis. It is a conjugate vaccine and will contain purified capsular polysaccaride, and either toxoid from tetanus or diptheria, or the outer membrane protein of N. meningitidis.
Haemophilus influenzae type B
This vaccine consists of hep B surface antigen that is produced in yeast using recombinant DNA technology. It can be combined with Hep A in the vaccine Twinrix.
Hepatitis B vaccine
This vaccine consists of inactivated Hepatits A virus.
Hepatitis A vaccine
This variant of the flu vaccine has inactive viral antigens.
Fluzone, Fluvirin
This variant of the flu vaccine uses live virus.
Flumist
This vaccine consists of the bacteria meningitis and S. pneumoniae, it is made of pneumococcal conjugates, either polysaccharides to protein (PCV7 or Prevnar) or unconjugated polysaccharide vaccine (Pneumovax-23).
Pneumococcal infection vaccines
This vaccine is made of the bacteria meningitis. There is a meningococcal conjugate vaccine (MCV4, Menactra) and a meningococcal polysaccharide vaccine (Menomume)
Meningococcal infection vaccines
This is a live oral pentavalent vaccine, goes by the names of Rotorix and Rototeq. It vaccinates against the 5 most common serotypes.
Rotovirus vaccine
This vaccine contains virus like particles of 4 types - 16, 18, 6, and 11. It protects against cervical, vulvar, vaginal, and anal cancer and warts.
Gardasil
This vaccine only has 2 serotypes, 16 and 18 and protects against cervical cancer.
Cervarix
This immunosuppressant drug functions by suppressing the production of IL-2, interferon gamma, and other cytokines. It binds to cyclophilin and inhibits calcineurin. It is used to prevent the rejection of organ transplants and for some autoimmune diseases such as RA and psoriasis. Adverse effects do not include bone marrow suppression but do include nephrotoxicity, infection, hepatotoxicity, lymphoma, hypertension, tremor, hirsutism, gynecomastia, hyperkalemia, anaphylaxis and it is embryotoxic and fetotoxic.
Cyclosporine (Sandimmune)
Name the five types of immunosuppressants.
calcineurin inhibitors, mTOR inhibitors, glucocorticoids, cytotoxic drugs, antibodies
What is the connection between phenytoin, phenobarbitol, carbamazepine, and rimfampin in regards to cyclosporine?
they all decrease cyclosporine levels
What is the connection between ketocanozole, erythromycin, amphotericin B, and cyclosporine?
These are all drugs that can increase cyclosporine levels
What is the connection between NSAIDS, amphotericin B, aminoglycerides, and cyclosporine?
These drugs are all nephrotoxic and shouldn’t be given with cyclosporine because renal damage will be intensified.
What does grapefruit juice do to cyclosporine levels?
increases them by 50-200% because it inhibits cyclosporine metabolism
This drug has a similar MOA to cyclosporine but binds to FKB12 to inhibit calcineurin. It is more effective than cyclosporine but also more toxic. It is used for the prophylaxis of organ rejection (liver or kidney transplant). Adverse effects include nephrotoxicity, neurotoxicity, GI effects, hypertension, hyperkalemia, hyperglycemia, hirsutism, and gum hyperplasia. It interacts with agents that inhibit CYP3A and they will increase levels of the drug (erythromycin, ketocanozole), and grapefruit juice will also cause an increase. NSAIDS will injure the kidneys more when given with this drug.
Tacrolimus (Prograf)
This class of drugs works by inhbiting an enzyme known as mammalian target of rapamycin. It is a protein kinase that helps regulate cell growth, proliferation, and survival.
mTOR inhibitors
This drug has a similar structure to Tacrolimus and binds to FKB12 but has a different mechanism in that it suppresses T cells. It is used only for renal transplant rejection and in conjunction with cyclosporine and glucocorticoids. Adverse effects include increased risk of infection, elevated cholesterol and triglycerides, risk of renal injury, severe complications in lung and liver recipients, rash, acne, anemia, thrombocytopenia, diarrhea, and hypokalemia. Rat studies showed death and low birth weight with pregnancy.
Sirolimus (Rapamune)
This drug is used for the prevention of organ rejection, and for renal and other cancers. It’s MOA is that it is a mTOR inhibitor like Sirolimus and utilizes T cell suppression. Adverse effects are peripheral edema, constipation, hypertension, nausea, anemia, UTIs, and hyperlipidemia. Effects were shown with pregnancy and lactation in rats. It interacts with drugs that inhibit or induce CYP3A4, high fat foods increase absorption, and grapefruit juice increases drug levels.
Everolimus (Zortress)
This drug suppresses immune response through the lysis of antigen activated lymphocytes, suppression of lymphocyte proliferation, and sequestration of lymphocytes in extravascular locations. It also reduces the production of IL-2 and the response of T-cells to IL-1. They are used for transplant rejection suppression, asthma treatment, and autoimmune disorders like SLE, MS, and RA. You need a high dose for immunosuppression (500-1500mg). Adverse effects include increased risk of infection, thinning of the skin, bone dissolution (with fractures), impaired growth in childrean, and suppression of the HPA axis.
Prednisone
This drug suppresses cell mediated and humoral immunity responses (inhibit proliferation of T and B cells) and is converted to mercaptopurine with inhibits DNA synthesis. It is an adjunct treatment for transplants (with cyclosporine and prednisone) and can be used with some autoimmune disorders (experimental with SLE and MG). Adverse effects include neutropenia, thrombocytopenia, teratogenic and mutagenic in animals, and neoplasms (tumors) with long term use.
Azathioprine (Imuran)
What drug class do the following drugs belong to: methotrexate, mitoxantrone, and cyclophosphamides.
cytotoxic drugs
This drug binds to CD3-R and blocks T cell function. It is used to prevent the rejection of transplants (liver, kidney, and heart) and to deplete T cells prior to a bone marrow transplant. Adverse effects are mild and include fever, chills, dyspnea, chest pain, nausea, vomiting, and possible anaphylactic reactions.
Muromonab-CD3 (Orthoclone OKT3)
These two drugs and monoclonal antibodies that block IL-2 receptors and thus block the activation of T cells. They are used for the prophylaxis of acute organ rejection (renal transplant)
Basiliximab (simulect) and Daclizumab (Zenapax)
This drug is an equine antithymocyte globulin obtained by shooting up a horse with Human T cell lymphocytes. It is given with azathioprine and glucocorticoids and is used to prevent rejection of renal transplants and for aplastic anemia.
Lymphocyte immune globulin (Atgam)
This drug is used to prevent reactions in Rh negative women around 28 weeks of gestation through 72 hours after delivery.
Rho(D) immune globulin (RhIG)
This chemical is responsible for the regulation of the allergic response. It dilates small blood vessels, increases capillary permeability and causes constriction of the bronchi. It can also stimulate gastric secretion. It is present in almost all tissue (skin, lungs, GI tract), and is stored in mast cells, basophils, and neurons. It can be released in allergic responses and in nonallergic responses.
histamine
What is phase 1 of the release of histamine in the allergic response?
The formation of IgE by the immune system.
What is phase 2 of the release of histamine in the allergic response?
IgE binds to mast cells
What is phase 3 of the release of histamine in the allergic response?
the allergen binds to IgE and causes the mast cell to release histamine
Which type of histamine receptor is activated if the effects are vasodilation, increased capillary permeability, bronchoconstriction, CNS effects, and itching, pain, and secretion of mucus?
H1 receptor
Which type of histamine receptor is activated if the effect is the secretion of gastric acid in the parietal cells of the stomach? This can cause ulcers.
H2 receptor
The first generation H1 antagonists chlorpheniramine and brompheniramine (Dimetapp) are of what type?
alkylamines
The first generation H1 antagonist diphenhydramine (benadryl) are of which type?
ethanolamines
The first generation H1 antagonist promethazine (phenergan) is of which type?
phenothiazines
The first generation H1 antagonist hydroxyzine (Vistaril) is of which type?
piperazines
The first generation H1 antagonists Azatadine and Phenindamine (Nalohist) are of what type?
piperidines
What are the two H1 antagonists that are used for motion sickness and exert their effects by blocking H1 receptors and M-receptors in the neuronal pathway (vestibular apparatus to the vomiting centers)?
Promethazine (Phenergan) and Dimenhydrinate (Dramamine)
This class of drugs work by blocking the action of histamine. The peripheral effects include the reduction of dilation, edema, itching, pain, and mucus secretion. The CNS effects include drowsiness, but also stimulation at high doses. These drugs are used for mild allergies, severe allergies (limited benefits), motion sickness, insomnia, and the common cold. Adverse effects are CNS depression and sedation, dizziness, confusion, fatigue, GI effects, and anticholinergic effects. If taken with CNS depressants there will be increased depression.
H1 antagonists - first generation
This class of drugs are nonsedating and don’t cross the BBB. The synergism with alcohol and other CNS depressants is low and it is largely devoid of anticholinergic effects. They cost 20x more than first generation antihistamines.
H1 antagonists - second generation
The following drugs all belong to what class: fexofenadine (allegra), cetirizine (zyrtec), lortidine (claritin, tavist ND, alavert), desloratidine (clarinex), Azelastine (Astelin)
H1 antagonists - second generation
This substance is distributed in all tissues and is responsible for housekeeping chores. It protects gastric mucosa by producing prostaglandins, and supports renal function through prostaglandins, as well as promotes platelet aggregation by producing thromboxane. Inhibiting it often results in harmful effects like bleeding, ulceration and renal impairment, but can be beneficial by protecting from myocardial infarction by preventing platelet aggregation.
Cyclooxygenase 1 (COX1)
This substance is only found at the site of tissue injury, brain, kidneys, blood vessels, and colon. It mediates inflammation, sensitizes receptors to painful stimuli at sites of injury. In the brain it brings on fever and the perception of pain, and in the kidney it supports renal function by increasing perfusion and renal dilation. Inhibition of this substance is largely beneficial because it suppresses inflammation, alleviates pain and reduces fever, and protects from colon cancer. The adverse effects of inhibition are renal impairment (HTN and edema) and possible MI and stroke.
Cyclooxygenase 2 (COX2)
Name three NSAIDs which are first generation and inhibit cox 1 and cox 2.
aspirin, ibuprofen, naproxen
Name the second generation NSAID that inhibits cox 2 only.
Celecoxib (Vioxx, Bextra)
This drug is a nonselective and irreversible inhibitor of cyclooxygenases, it is used as an analgesic, antipyretic, and antiinflammatory for conditions such as arthritis, pain and fever reduction due to it’s COX2 inhibition. It is used in the prevention of MI, stroke, and angina due to the suppression of platelet aggregation due to COX 1 inhibition. It is used for dysmenorrhea, cancer prevention when used long term and at high doses, and the prevention of Alzheimer’s disease. It has a short halflife and is converted to salicylic acid which is 80-90% bound to albumin and is excreted in the urine.
aspirin
Adverse effects of this drug include GI effects such as gastric distress, heartburn, and nausea, bleeding, renal impairment with reduced urine output. salicylism is also possible which is marked by tinnitus, sweating and dizziness at high doses, and acid-base imbalances in the plasma due to CNS stimulation of breathing which causes a loss of CO2 and respiratory alkalosis. It can also cause Reye’s syndrome which involves encephalopathy and fatty liver degeneration when given to children with viral illnesses like the flu or chickenpox. There can also be hypersensitivity reactions like anaphylaxis, but this is usually seen in asthma patients and patients with rhinitis. It interacts with warfarin and intensifies the anticoagulant effect. When combined with glucocorticoids it causes gastic ulceration and when combined with alcohol it causes gastric bleeding. When combined with ibuprofen the ibuprofen blocks the access of this drug to COX1 in platelets and reduces the antiplatelet effects. When combined with ACE inhibitors and ARB’s it leads to impaired renal function.
aspirin
This class of drugs is aspirin-like with fewer GI, renal, and hemorrhagic effects than aspirin. They inhibit COX1 and COX2 reversibly, unlike aspirin. They are used for arthritis and osteoarthritis and do not protect against MI or stroke. There are 20+ drugs like this available and they are all similar. Propionic acid derivatives such as ibuprofen (advil, motrin), naproxen (naprosyn), Alleve, Naproxen plus Iansoprazole, Fenoprofen, Flurbiprofen, Ketoprofen, and Oxaprozin are some of them. Also Indomethicin (indocin), Diclofenac (Voltaren, Cataflam), Diclofenac with misprostol, and Piroxicam (Feldene)
Other Non-aspirin 1st generation NSAIDs
This drug is a second generation COX2 inhibitor, it has fewer adverse effects than the first generation and the first one was approved in 1998. It is the last choice drug for long term pain management due to the increased risk of MI and stroke. It is used for osteoarthritis, RA, ankylosing spondylitis, acute pain, dysmenorrhea, familial adenomatous polypopsis (inherited colorectal cancer). Adverse effects include stroke and MI, dyspepsia and ulcers, abdominal pain, renal toxicity (impaired function), sulfonamide (sulfur) allergy, and in pregnancy premature closure of the ductus arteriosis in the third trimester.
Celecoxib (Celebrex)
Name the two COX 2 inhibitors that were initially approved and then pulled off the market due to more cardiovascular events at high dosage such as stroke and MI was shown to occur in further research.
Vioxx (pulled in 2004) and Bextra (pulled in 2005)
This drug inhibits prostaglandin synthesis in the CNS and has minimal effects on the periphery. It’s therapeutic actions include analgesic, antipyretic effects and it is preferred for children because it doesn’t cause Reyes syndrome. Adverse effects include hepatotoxicity, no antiinflammatory/gastric ulceration/ adverse effects on platelets, overdose causes hepatic necrosis. Mucomyst can be used as an antidote if overdose occurs. It interacts with alcohol and this increases the hepatotoxicity and when given with warfarin it increases bleeding.
Acetaminophen (Tylenol)
This type of hypertension has no identifiable cause but it is a chronic, progressive disorder that is seen in people aged 25-74 . It is lifelong and is treatable but not cured.
Primary (essential) hypertension
This type of hypertension has an underlying causes that is treatable, such as renal failure, thyroid issues, cushing’s syndrome, primary hypoaldosteronism, or pheochromocytoma.
secondary hypertension
What are some consequences of hypertension?
heart disease (MI, heart failure, angina pectoris), chronic kidney disease, stroke, peripheral artery disease and retinopathy.
What are some lifestyle modification to control hypertension?
weight loss, sodium restriction, DASH eating plan (fruits, vegetable, low fat, low cholesterol), alcohol restriction, aerobic exercise, smoking cessation, and maintenance of K+ and Ca2+ intake.
Name two antihypertensive drugs that are beta-adrenergic blockers.
propanolol and metaprolol
Name two antihypertensive drugs that are alpha 1 blockers.
doxazosin and terazosin
Name two antihypertensive drugs that are alpha/beta blockers.
carvedilol and labetalol
Name two antihypertensive drugs that are centrally acting alpha 2 agonists.
clonidine and methyldopa
Name three antihypertensive drugs that are adrenergic neuron blockers.
guanethidine, guanaderal, and reserpine
This class of diuretic drugs and its prototype are first line treatment for HTN. They lower BP through the reduction of blood volume and the reduction of vascular resistance. The main adverse effect of these drugs is hypokalemia, but also could include dehydration, hyperglycemia, and hyperuricemia. These drugs are cheaper and superior to calcium channel blockers and ACE inhibitors as monotherapy.
thiazide diuretics (hydrochlorothiazide)
This class of diuretics produces greater diuresis than thiazides, usually to a greater extent than what is necessary or desirable. This makes them a less routinely used and indicated only for patients who need greater diuresis than can be achieved with thiazides or who have a low GFR. They work by lowering blood volume and promoting vasodilation. Adverse effects include hypokalemia, dehydration, hyperglycemia, hyperuricemia, and hearing loss.
high ceiling loop diuretics (furosemide)
This type of drug has a small diuretic effect and only modest hypotensive effects, however they can be used to balance potassium loss by thiazides and loop diuretics. The main adverse effect is hyperkalemia, thus drugs in this class shouldn’t be combined with one another or with potassium supplements, ACE inhibitors, angiotensin II receptor blockers, or aldosterone antagonists…all of which promote hyperkalemia.
potassium sparing diuretics (spironolactone)
This direct acting vasodilator causes selective dilation of the arterioles which decrease afterload, reduces cardiac work, and increases tissue perfusion. It has little to no effect on veins. Its MOA is that it works directly on vascular smooth muscle. It is used therapeutically for essential hypertension (almost always combined with beta blocker and diuretic), hypertensive crisis (it will rapidly lower BP but should be given in small incremental doses), and heart failure to reduce afterload (in prolonged therapy tolerance builds). Adverse effects include reflex tachycardia (combined with beta blockers to reduce this), increased blood volume (due to retention of Na and H2O), and SLE like syndrome including muscle pain, joint pain, fever, nephritis, pericarditis, and the presence of antinuclear antibodies. Headache, dizziness, and fatigue are also possible.
Hydralazine (Apresoline)
This direct acting vasodilator if more intensive than hydralazine and has more severe adverse effects so it is reserved for severe hypertension. It selectively dilates arterioles. It’s MOA is that it is metabolized to Minodixil sulfate which opens up potassium channels in vascular smooth muscles and hyperpolarizes them. It is used for severe hypertension (with beta blockers and diuretics) and in a topical formulation to promote hair growth (Rogaine). Adverse effects include reflex tachycardia (needs a beta blocker), sodium and water retention (diuretic can be used), hypertrichosis (excessive hair growth), and rarely pericardial effusion (fluid accumulation beneath the pericardium)
Minoxidil (Loniten)
This drug is the fastest acting antihypertensive agent and is used for hypertensive emergencies. It is administered via IV infusion and its onset is immediate. It’s MOA is that it causes venous and arteriole dilation. Adverse effects include excessive hypotension (if given fast, BP should be monitored closely), cyanide poisoning (in patients with liver disease and low cofactor used to process the cyanide byproducts (if this is the case administer slowly and with the cofactor thiosulfate), Thiocyanate toxicity can still develop which can cause disorientation, psychotic behavior and delirium. Long term levels should be monitored and these chemicals are all eliminated over several days by the kidneys.
Sodium Nitroprusside (Nitropress)
These class of drugs reduce the level of angiotensin II by inhibiting ACE. They also increase the level of bradykinin by inhibiting kinase II. Tissue or local angiotensin II production doesn’t always involve ACE, so these drugs don’t have any effect on this production. Reduced angiotensin II leads to vasodilation, decreased blood volume, decreased cardiac and vascular remodeling, potassium retention, and fetal injury. Increased bradykinin leads to vasodilation, cough, and rarely angioedema.
angiotensin converting enzyme inhibitors (ACE inhibitors)
This ACE inhibitor works via reduction in angiotensin II. It is used for hypertension (moreso 20 years ago), heart failure (because it lowers arterial tone and improves regional bloodflow and increases carbon monoxide. Myocardial infarction, diabetic and nondiabetic nephropathy (end stage renal disease) as it slows the progression. Adverse effects include first dose hypotension, hyperkalemia, cough, angioedema, dysgeusia, rash, renal failure, neutropenia, and fetal injury in the II and III trimesters. Drug interactions include diuretics (intensify 1st dose hypotension), antihypertensive agents (additive hypotensive effects), drugs that increase K+ levels (hyperkalemia increased), Lithium (this drug increases Li levels), and NSAIDs (reduce antihypertensive effects)
ACE inhibitors - Captopril (Capoten)
This drug was initially used for hypertension but is also used for heart failure, diabetic neuropathy, MI, and stroke prevention. It’s MOA is that it blocks access of angiotensin II causing dilation of arterioles and veins. It also prevents angiotensin II from inducing pathologic changes in cardiac structure. It decreases the release of aldosterone which leads to increased renal excretion of sodium and water and reduced potassium excretion. There is no increase in bradykinin level (no cough). Adverse effects include angioedema (lower incidence) by increase in bradykinin synthesis (indirect mechanism), fetal harm (in 2 or 3 trimester), renal failure (with bilateral renal artery stenosis), and a small risk of cancer. It interacts and has an additive effect with other antihypertensives.
angiotensin II receptor blockers - Lozartan (Cozaar)
This drug is the only one available in it’s class and was approved for HTN in 2007. It’s MOA is that it tightly binds to renin and prevents the formation of angiotensin I. It is used for hypertension along with other antihypertensive drugs. Adverse effects include angioedema and cough, diarrhea, abdominal pain and dyspepsia at high doses, hyperkalemia when used with other drugs, and fetal injury and death.
direct renin inhibitors - Aliskiren (Tekturna)
This drug was approved in 2002 and it’s MOA is that it selectively blockades aldosterone receptors. It is used for hypertension and is superior to Losartan (ARB) and takes 4 weeks to reach its max effect. It can also be used for heart failure (improves symptoms and reduces hospitalization). The main adverse effect if hyperkalemia. It shouldn’t be used with potassium supplements, salt substitutes, or potassium sparing diuretics (caution when used in combo with ACE inhibitors or ARBs), inhibitors of CYP3A4 (erythromycin, saquinivir, ketoconazole) increase the levels of the drug, this drug can also increase the level of lithium.
Eplerenone (Inspra) - aldosterone antagonist
This drug is older than Eplerenone, its MOA is that it blocks aldosterone receptors and binds with receptors for other steroid hormones (glucocorticoids, progesterone, and androgens). It is used for hypertension and heart failure. Adverse effects include hyperkalemia, gynecomastia, menstrual irregularities, impotence, hirsutism, and deepening of the voice.
Spironolactone (Aldactone)
This element regulates the contraction of vascular smooth muscle by entering and initiating contraction, but has no effect on veins. In the heart it helps regulate the myocardium and the SA and AV nodes (increased discharge, increased HR and conduction), and channels for it are coupled to beta1 adrenergic receptors in the heart. This means that activation of beta1 receptors enhances the influx of this chemical and block of beta1 receptors and the channel consequently have the same effect.
calcium
This class of drugs work by blocking calcium entry and has the greatest effect on the heart and smooth muscles. There are three major sub groupings, dihydropyridines (nifedipine), phenylalkylamine (verapamil), and benzothiazepine (dilitiazem).
calcium channel blockers (calcium antagonists)
This phenylalkylamine blocks calcium channels in blood vessels and the heart. It causes hemodynamic effects such as vasodilation, reduced heart rate (SA node) and decreased conduction (AV node), as well as decreased force of contraction (myocardium). Indirect effects include sympathetic activity but there is little to no effect on cardiac performance. Therapeutic uses include angina pectoris (vasodilation), essential HTN, cardiac dysrhytmias (slows ventricular rate), and migraine (investigational). Adverse effects include constipation (block in smooth muscle), dizziness, facial flushing, headache, edema of ankles and feet (all secondary to vasodilation), gingival hyperplasia, and heart block (not to be used with 2nd/3rd AV block).
Verapamil (Calan, Covera-HS, Isoptin, Verelan)
This dihydropyridine acts mainly on smooth muscle and causes vasodilation by blocking calcium channels. The net effect is lowered BP, increased coronary perfusion, increased heart rate and contractile force (baroreceptor reflex). The baroreceptor reflex is only a concern with the fact acting and not the sustained release formulations. It is used for angina pectoris (combined with a beta blocker to prevent reflex cardiac stimulation), HTN (sustained release form), and to suppress preterm labor (investigational). Adverse effects include flushing, dizziness, headache, peripheral edema, gingival hyperplasia, and reflex tachycardia (beta blockers are added). Again, beta adrenergic blockers are used to decrease the adverse cardiac effect. At toxic doses this drug loses its selectivity and the heart is also effected.
Nifedipine (Adalat, Nifedical, Nifediac, Procardia)
This classification of calcium channel blockers acts primarily on the arterioles.
dihydropyridines
This classification of calcium channel blockers works on the arterioles and on the heart.
phenylalkylamines
All of the following drugs are administered by IV for a specific condition. What is this condition and how is it defined? The drugs are sodium nitroprusside, Fenoldopam (corlopam), labetalol (trandate), diazoxide (hyperstat IV), and Clevidipine (Cleviprex).
hypertensive emergencies, which is defined as diastolic BP greater than 120 mmHg.
This pathology is occurs when the heart isn’t able to pump sufficient blood to meet metabolic needs. It is characterized by inadequate tissue perfusion (fatigue, shortness of breath, exercise intolerance), signs of volume overload (venous distention, peripheral and pulmonary edema). Major underlying causes include chronic hypertension and myocardial infarction. Other causes include valvular heart disease, congenital heart disease, dysrhythmias, and aging of the myocardium.
congestive heart failure (CHF)
This type of drug is the first line treatment for congestive heart failure. Their MOA is that they reduce blood volume, decrease venous and arterial pressure (afterload), decrease pulmonary and peripheral edema, decrease cardiac dilation. The benefits are limited to symptom reduction and there are three different types.
diuretics
This type of diuretic causes moderate diuresis and is widely used when edema isn’t great. They are ineffective when GFR is low and CO is greatly reduced. Hypokalemia is an adverse effect.
Thiazide diuretics - hydrochlorothiazide (hyrdodiuril)
This type of diuretic is the drug of choice for severe heart failure. It causes profound diuresis and is reserved for rapid effects (can be used in low CO or low GFR patients). Hypokalemia and severe hypotension are possible adverse effects.
High ceiling (loop) diuretics - furosemide (Lasix)
This type of diuretic produces modest diuresis and blocks aldosterone receptors. It can counteract potassium loss by the other two types of diuretics since hyperkalemia is an adverse effect.
potassium-sparing diuretics - spironolactone (aldactone)
What other three classes of drugs are used after diuretics to treat CHF?
Drugs that inhibit RAAS (ACE inhibitors, ARBs, Aldosterone antagonists, and direct renin inhibitors, beta blockers, and inotropic agents.
This drug is a cardiac glycoside and comes from a naturally occurring compound (purple foxglove/ digitalis purpurae). Pharmacologically profound effects are seen on the electrical and mechanical properties of the heart. Potassium levels must be kept within the normal physiologic range because potassium competes with this drug for the pump. The benefits of increased CO include decreased sympathetic tone, increased urine output, and decreased renin release. This drug is a second line treatment because of a low TI. Adverse effects include altering the electrical activity of the heart and potentially causing dysrhythmias, hypokalemia (use of diuretics : thiazides) which increases the inhibition of the Na+/K+ pump that this drug effects. Non cardiac adverse effects include GI issues, fatigue, and visual disturbances. There is also a slight increase in death for women. Drug interactions include diuretics (K levels low cause an increase in risk of dysrhythmias), ACE inhibitors and ARBs (increase K and reduce drug effects), sympathomimetics (increase heart rate -can be good or bad), and verapamil (increase levels of this drug).
Digoxin (Lanoxin, Lanoxicaps, Digitek)
Isosorbide dinitrate plus hydralazine, nitroglycerin, sodium nitroprusside (Nitropress), and Nesiritide (Natrecore) are all meds used to treat CHF…what kind of drugs are they?
vasodilators (other than ACE inhibitors and ARBs)
What are the two types of dysrhythmias?
Tachydysrhythmia and Bradydysrhythmia
Disturbances of automaticity (impulse formation) caused by hypoxia, electrolyte imbalance, cardiac surgery, MI, reduced coronary bloodflow, and antidysrhythmic drugs, and disturbances in conduction like with an AV block (1 degree - PR interval delay, 2 degree - some impulses pass through and some not, and 3 degree - no conduction and complete block) are the two fundamental causes of what condition?
dysrhythmias
This class of drugs for dysrhythmias has a similar action and structure to local anesthetics. (local anesthetic antidysrhythmic drugs). It;s MOA is to descrease conduction velocity in the atria, ventricles, and His-purkinje system. Class 1a agents delay repolarization (quinidine), class 1b agents accelerate repolarization (lidocaine), and class 1c are pronounced prodysrythmic drugs. Other class 1’s include moricizine.
Class 1: Sodium channel blockers
This class 1 agent comes from the S, American cinchona tree and is used for supraventricular and ventricular dysrhythmias. It’s MOA is that it blocks sodium channels and slows impulse conduction, and delays repolarization by blocking K channels. Adverse effects include diarrhea, chinchonism (tinnitus, hadache, nausea, vertigo, and disturbed vision on the first dose), cardiotoxicity (at high concentrations - sinus arrest, AV block, ventricular dysrhythmias - wider QRS and QT prolongation), arterial embolism (during atrial fib. thrombi forms and dislodges into arteries - warfarin treatment 3-4 weeks prior), alpha-adrenergic blockade resulting in hypotension (IV than oral), and hypersensitivity reactions (rare). Doubles digoxin levels (last DOC for digoxin induced dysrhythmias)
Quinidine
This class II drug for dysrhythmias in a nonselective beta-adrenergic antagonist. It is used for dysrhythmias (due to excessive sympathetic stimulation) and supraventricular tachydysrhythmias which the drug helps by suppressing excessive discharge and slowing the ventricular rate (decreased conduction through the AV node causing a prolonged PR interval on an ECG). Adverse effects include heart block (AV block), heart failure, sinus arrest, hypotension (secondary to reduced CO), and bronchospasm (beta-2 receptor block in asthma patients.
Class II Beta Blocker - Propanolol (Inderal)
This class III drug for dysrhythmias is for short term use only. It delays the repolarization of fast potentials and prolongs the QT interval due to ventricular repolarization delay. It’s therapeutic use is that it blocks the K+ channels in purkinje and ventricular muscle and can be used for ventricular fibrillation and ventricular tachycardia short term for patients who have been refractory to conventional therapy.
Class III Potassium Channel Blockers - Bretylium
These two drugs are both class IV drugs for dysrhythmias. Their type of blockage in the heart has 3 effects that are similar to beta blockade and include reducing SA nodal automaticity, delaying AV nodal conduction (prolonged PR interval) and reducing myocardial contractility. They can be used to slow the ventricular rate (with atrial fibrillation or atrial flutter) and to terminate SVT (caused by AV nodal reentrant circuit). Adverse effects include bradycardia, AV block, heart failure, hypotension and peripheral edema (block of Ca in vascular smooth muscle and vasodilation), constipation (block of Ca in smooth muscles). There are a couple of drug interactions, digoxin levels will be elevated possibly causing digoxin toxicity and increased AV block. The drug also interacts with beta blockers and increases the heart suppressant effect and increasing the risk of bradycardia, AV block, and heart failure.
Class IV calcium channel blockers verapamil and diltiazem
This “other” antidysrhythmic drug has a short half life and is administered IV. It decreases the automaticity in the SA node, slows conduction through the AV node, and causes a prolongation of the PR interval (due to delayed AV conduction). It is used for the termination of paroxysmal SVT and is not effective for atrial flutter, atrial fibrillation or ventricular dysrhythmias. Adverse effects are short (less than a minute) but include sinus bradycardia, dyspnea (bronchoconstriction) hypotension (vasodilation), and facial flushing. Drug interactions include methylxanthines which block adenosine receptors, and dipyridamole which blocks the cellular reuptake of adenosine and increases the level of this drug.
Adenosine (Adenocard)
This pathology is the leading killer of men and women in the US. It is caused by a thickening of the coronary arteries (atherosclerosis). Moderate pathology leads to angina pectoris and severe pathology leads to myocardial infarction.
coronary artery disease (CHD)
This substance is directly related to the risk of developing CHD, it is transported by plasma lipoproteins in blood. There are six major lipoproteins, 3 of which are clinically relevant; LDL and triglyceride (apo B100) and HDL (apo A1 and A2).
cholesterol
Total cholesterol should be under what level?
240 mg/dL is high risk
HDL cholesterol should be above what level?
> 40 mg/dL, >/= 6o is considered high
LDL cholesterol should be below what level?
190 is very high
What level of triglycerides is considered high risk?
200-499, >500 is very high risk
The TLC diet, weight control, exercise, and smoking cessation are all what in regard to high LDL cholesterol?
therapeutic lifestyle changes (first line therapy)
Drugs like HMG-CoA reductase inhibitors, bile-acid sequestrants, nicotinic acid (niacin), fibrates, and other drugs are all second line treatments for what condition?
high LDL cholesterol
This condition is associated with the risk of CHD and type II diabetes. It is diagnosed when 3 or more of the following are present: abnormal obesity (waist circumference >40 and >35), high blood glucose (fasting: 110 mg/dl or higher), high triglycerides (150 mg/dl or higher), low HDL (below 40 or 50 mg/dl), and hypertension (130/85). Weight reduction and increased exercise are recommended.
metabolic syndrome
These drugs are the most effective for lowering LDL and their MOA is to block cholesterol synthesis, increase the number of LDL receptors on liver cells to help remove LDL, and decrease apo B-100 (reduce VLDL and elevate HDL). It’s used for hyperlipidemia, CV disorder (primary and secondary) and post MI, and also for diabetes. They could potentially be used for alzheimer’s parkinson’s, MS, glaucoma, macular degeneration, RA, kidney disease, and even cancer. Adverse effects include headache, rash, GI disturbances, myopathy and rhabdomyolysis (rare), hepatotoxicity (rare), and peripheral neuropathy.
HMG-CoA Reducatse Inhibitors (Statins) - Atorvastatin (lipitor) and Simvastatin (zocor)
This statin drug is newer but has more serious adverse effects.
rosuvastatin (crestor)
This drug reduces LDL and TG levels and increases HDL levels better than any other drug. It’s MOA is that it decreases production of VLDL’s (inhibition of lipolysis in adipose tissue). Adverse effects give it limited clinical utility and include skin flushing and itching with is reduced by taking aspirin, GI issues such as nausea, vomiting, and diarrhea, heaptotoxicity (long acting one), hyperglycemia, and gouty arthritis.
Nicotinic Acid (Niacin)
This combination drug in a clinical trial lowered LDL 45%, raised HDL 41%, and lowered TGs 42%.
Niacin/Lovastatin (Advicor)
This drug was approved in 2000 and is a drug of choice. It’s MOA is that it prevents the absorption of bile acid (drug complexes with bile and other material excreted) and this causes a reduction in LDL (increase in LDL-receptor and removes LDL) but also increases VLDL (meaning the drug isn’t good for people with increased VLDL). It is used with diet and exercise to reduce LDL cholesterol, can be used as monotherapy or with statins. Adverse effects include constipation, bloating, indigestion, and nausea.
bile acid sequestrants - Colsevelam (Welchol)
This drug is indicated primarily for hypertriglyceridemia and has no effect on LDL. It reduces high levels of plasma triglycerides (VLDLs). It’s MOA is that it activates PPAR-alpha (peroxisome proliferator activated receptor) in brown and adipose tissue which leads to increase synthesis of LPL and reduced apo-c III production (inhibits LPL). this leads to lower VLDL levels and higher HDL levels (increase apo A1 and AII). Adverse effects include rashes, nausea, abdominal pain, bloating, gallstones, myopathy, and liver injury (hepatotoxicity)
Fibric Acid Derivatives (Fibrates) - Gemfibrozil (Lopid)
This drug was approved in 2008 and is an active metabolite of fenofibrate (only fibric acide derivative approved with statin). They can also cause myopathy and should be given with care.
Fenofibric acid (Trilipix)
This drug was approved in 2002 and it’s MOA is to inhibit cholesterol absorption. It acts on cells of the brush border of the small intestine. It lowers the total, LDL, TG and apo-B and elevates HDL. It is combines with diet modification or can be used as monotherapy. If combined with statin drugs (liver damage can occur and transaminase levels should be monitored). Adverse effects are myopathy, rhabdomyolysis, hepatitis, pancreatitis, thrombocytopenia.
Ezetimibe (Zetia)
These drug combinations Niacin/Lovastatin (advicor), simvastatin/ezetimibe (vyotorin), pravastatin/aspirin (pravigardPAC), and atorvastatin/amlodipine (caduet) are used for what?
altering plasma lipid levels
What are some other products used to alter plasma lipid levels?
fish oil with omega 3 fatty acidss, plant stanol and sterol esters (promise and benecol), estrogen (reduces LDL and increases HDL), cholestin (made of rice fermented yeast and has 7 HMG-CoA reductase inhibitors and lovastatin in it, get it at health stores)
This pathology is characterized by sudden pain beneath the sternum that often radiates to the arms and it occurs when oxygen supply is insufficient to meet oxygen demand. The goals of drug therapy for this condition are to prevent MI and death by using cholesterol lowering drugs and antiplatelet drugs, and the prevention of myocardial ischemia and pain.
angina pectoris
What are the three families of antianginal agents?
organic nitrates, beta blockers, and calcium channel blockers
This type of angina is triggered by an increase in physical activity.
chronic stable angina (exertional)
This type of angina is caused by coronary artery spasm which restricts blood flow. It can occur anytime.
variant angina (Prinzmetal’s or vasospastic angina)
This type of angina is a medical emergency and symptoms result from severe coronary artery disease. It includes vasospasm, platelet aggregation, and transient coronary thrombi or emboli.
unstable angina
This drug for angina pectoris has been in use since 1879. It is a vasodilator that increases cGMP formation. It has adverse effects including headaches, orthostatic hypotension, and reflex tachycardia. Tolerance builds rapidly over a single day (tachyphylaxis) due to the depletion of sulfhydryl groups in vascular smooth muscle. Drug interactions occur with hypotensive drugs (beta blockers, Ca channel blockers, diuretics, etc.) causing life threatening hypotension. Beta blockers and Ca channel blockers reduce the tachycardia produced by this drug. Phosphodiesterase type 5 inhibitors (viagra, cialis, and levitra) increase cGMP levels and can lead to life threatening hypotension.
Nitroglycerin (organic nitrates)
This type of revascularization therapy is used to increase bloodflow to ischemic areas of the heart and is the treatment of choice for multi-vessel disease. It is expensive and requires hospitalization with a longer stay.
coronary artery bypass graft surgery (CABG)
This revascularization therapy is an alternative to CABG and involves balloon angioplasty followed by stenting.
percutaneous coronary intervention (PCI)
This new drug was approved for angina pectoris and is the first drug approved in 25 years. It is approved for first line treatment despite QT interval issues and increased BP. It can be combined with other medications. It’s MOA is unknown but it reduces Na and Ca in myocardial cells.
Ranolazine (Ranexa)
This anticoagulant is rapid acting and is IV only. It occurs naturally in the lungs of cattle and intestines of pigs. It is used for pulmonary embolism (PE), evolving stroke, and massive deep venous thrombosis (DVT). Adverse effects include hemorrhage, thrombocytopenia induced by the drug, and hypersensitivity reactions. Protamine sulfate can be given for OD. The goal of antocoagulant therapy is to reduce blood coagulability to prevent thrombosis without having spontaneous bleeding. Activated partial thromboplastin time (aPTT) is a lab test used to measure coagulation. The normal value for the test is 40 seconds, when on this drug it will go to 60-80 seconds. It should be performed every 4-6 hours and then daily after dose is established.
Heparin
This drug is an oral anticoagulant and is a vitamin K antagonist (vitamin K can be used for OD). It blocks the biosynthesis of 4 clotting factors - VII, IX, X, and prothrombin. it is used for the long term prophylaxis of thrombosis (prevent ischemic attacks and MI). Adverse effects include hemorrhage and is is contraindicated in pregnancy and lactating women. It’s anticoagulant effects should be monitored using PT value (normal is 12 seconds). Drug interactions exist with drugs that increase anticoagulant effects such as (aspirin, tylenol, cimetidine, antibiotics), drugs that promote bleeding (anticoagulants, antiplatelet, aspirin, and glucocorticoids), drugs that decrease anticoagulant effects (carbamazapine, phenobarbitol, phenytoin, rifampin, vitamin K, and cholestyramine), heparin (inc. bleeding), aspirin (inc bleeding), non aspirin antiplatelet drugs, and acetaminophen (inhibits breakdown of this drug)
warfarin (coumadin)
This antiplatelet drug works by inhibiting cyclooxygenase.
aspirin (ASA)
This antiplatelet inhibits ADP-mediated aggregation, that is to say it is an ADP receptor antagonist.
Ticlopidine (Ticlid)
This antiplatelet drug is an adenosine diphosphate (ADP) receptor antagonist. Prasugrel (effient) is an investigational agent.
Clopidogrel (Plavix)
These are the msot effective antiplatelet drugs. They bring about reversible blockade of platelet GP IIb/IIIa receptors - they are antagonists at these sites.
Abciximab (ReoPro), Tirofiban (Aggrastat), and eptifibatide (integrilin)
This thrombolytic drug binds to plasminogen and increases plasmin, which degrades fibrin clots. It is used for acute coronary thrombosis (acute MI), deep venous thrombosis (DVT), and massive pulmonary emboli. Adverse effects include bleeding, antibody production because this drug is extracted from culture of streptococci, hypotension, and fever.
Streptokinase (Streptase)
Human tPA promotes conversion of plasminogen to plasmin
Atleplase (Activase)
A variant of human tPA - only approved for MI and had a longer half life and single IV.
Tenecteplace (TNKase)
This direct thrombin inhibitor was approved in 2010. It is compared to warfarin - it has a rapid onset, no monitoring, low risk, less drug-food itneractions, is predictable and the same does is used for all patients. It is an oral prodrug that is converted to dabigatran (active) by plasma esterases. It’s MOA is direct reversible inhibition of thrombin which prevents clots. It is used to prevent stroke and systemic embolism with atrial fibrillation. Adverse effects include bleeding (life threatening hemmorhage, recombinant factor VIIa or dialysis for treatment), dyspepsia and gastritis like symptoms. Drug interactions include drugs that inhibit p-glycoprotein (ketaconazole, amiodarone, verapamil, quinidine) cause bleeding due to increased drug levels.
Dabigatran Etexilate (Pradaxa)
This oral anticoagulant was approved in 2011 and doesn’t require laboratory monitoring. Patient who received this drug were found to be much less likely to experience DVT, VTE, PE, or death. It’s MOA is direct inhibition by binding to active center or Xa. It is used for the prevention of DVT and PE following knee and hip replacement surgery, and the prevention of stroke in patients in atrial fibrillation. Adverse effects include bleeding and spinal or epidural hematoma. Drug interactions include drugs that inhibit p-glycoprotein (ketaconazole, ritonavir) which increase drug levels and cause increased bleeding. Precautions should be utilized when giving to patients with impaired renal and hepatic functioning. It can also have pregnancy related hemorrhage and detrimental effects to the fetus.
Rivaroxaban (Xarelto)
