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160 Cards in this Set

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Local anesthetics are frequently administered in combination with:
a vasoconstrictor (typically epinephrine). The vasoconstrictor decreases blood flow (to delay absorption of the anesthetic) and also reduces the risk of toxicity.
The process by which a local anesthetic is metabolized depends on the class (ester or amide) to which it belongs:
Ester-type anesthetics are metabolized in the blood by enzymes known as esterases. In contrast, amide-type anesthetics are metabolized by enzymes in the liver
Adverse effects of local anesthetics:
CNS effects: local anesthetics can cause excitation followed by depression.

Cardiovascular effects: local anesthetics can affect the heart and blood vessels. They may suppress cardiac excitability and can therefore cause bradycardia, heart block, reduced contractile force, and cardiac arrest. In blood vessels, they cause vasodilation and hypotension

Allergic reactions

Labor and delivery
the prototype of the ester-type local anesthetics. The drug is not effective topically, and hence must be given by injection. It is available for injection in 1%, 2%, and 10% solutions. Administration in combination with epinephrine delays absorption. Systemic toxicity is rare because plasma esterases rapidly convert the drug to inactive, nontoxic products. However, being an ester-type anesthetic means that it poses a greater risk for allergic reactions
the prototype of the amide-type agents. It is one of today’s most widely used anesthetics. Lidocaine can be administered topically (cream, ointment, jelly, solution, aerosol, and patch) and by injection. Individuals who are allergic to ester-type anesthetics are not cross-allergic to lidocaine. In addition to its use in local anesthesia, lidocaine is employed to treat dysrhythmias.
an ester-type anesthetic. Described in 1884 by Sigmund Freud and Karl Koller, cocaine was the first local anesthetic. In addition to causing local anesthesia, cocaine has pronounced effects on the sympathetic and central nervous systems (due in large part to the drug’s ability to block uptake of NE by adrenergic neurons).
Cocaine is administered topically as a local anesthetic. It is employed for anesthesia of the ear, nose, and throat. Cocaine is readily absorbed, so its effects develop rapidly.
Cocaine produces generalized CNS stimulation. Moderate doses cause euphoria, reduced fatigue, and increased alertness. Excessive doses can cause seizures. CNS excitation is followed by CNS depression; respiratory arrest and death can result. Although cocaine does not seem to cause substantial physical dependence, psychological dependence can be profound.
Cocaine stimulates the heart and causes intense vasoconstriction (due to blockade of NE uptake at sympathetic nerve terminals on blood vessels). For this reason, the drug should never be given in combination with epinephrine or other vasoconstrictors. Central stimulation of the sympathetic nervous system and blockade of NE in the periphery causes hypertension, dysrhythmias, and angina. Cocaine poses a serious risk to patients with cardiovascular disease.
Injection types of local anesthetics include:
o Infiltration anesthesia is achieved by injecting a local anesthetic directly into the immediate area of surgery or manipulation
o Nerve block anesthesia is achieved by injecting a local anesthetic onto or near nerves that supply the surgical field, but at a site distant from the field itself
o Intravenous regional anesthesia is employed to anesthetize the extremities (but not the entire leg)
o Epidural anesthesia is achieved by injecting a local anesthetic into the epidural space of the spinal column (outside of the dura matter)
o Spinal (subarachnoid) anesthesia is produced by injecting a local anesthetic into the subarachnoid space. The most serious side effect of spinal anesthesia is hypotension
Balanced anesthesia
is a technique employed to compensate for the lack of an ideal drug. Drugs are combined in balanced anesthesia to ensure that induction is smooth and rapid, and that analgesia and muscle relaxation are adequate. The agents most commonly used to achieve these goals are:
1) Short-acting barbiturates (for induction of anesthesia)
2) Neuromuscular blocking agents (for muscle relaxation)
3) Opioids (for analgesia)
4) Nitrous oxide (for analgesia)
The molecular mechanism of action of inhaled anesthetics:
Though it is unclear, attention has shifted from nonspecific effects on neuronal membranes to selective alteration of synaptic transmission.
For many years, it was thought that inhalation anesthetics acted by disrupting the lipid bilayer of the neuronal membrane. By doing so, they suppressed axonal conduction and synaptic transmission.
More recent data suggests that inhalation anesthetics work by activating receptors for GABA, the principle inhibitory NT in the CNS. Increasing receptor sensitivity to GABA enhances transmission at inhibitory synapses. At excitatory synapses, inhalation anesthetics cause depression of the niconitic receptor, which is associated with memory and the perception of pain
Minimum alveolar concentration
an index of the potency of the inhalation anesthetic. MAC is defined as the minimum concentration of the drug in alveolar air that will produce immobility in 50% of patients exposed to a painful stimulus. A low MAC indicates high anesthetic potency.
Adverse effects to inhalation anesthesia:
Respiratory and cardiac depression
Increased sensitization of the heart to catecholamines
Malignant hyperthermia
Aspriration of gastric contents
Toxicity may develop in operating room personnel
Preanesthetic medications:
Anticholinergic drugs
Neuromuscular blocking agents
Post-anesthetic medications:
Muscarinic agonists
Nitrous oxide
Nitrous oxide has a very low anesthetic potency but a very high analgesic potency. It is almost impossible to produce surgical anesthesia employing NO alone. When administered alone, NO is employed for analgesia.
A) Halothane [Fluothane] is the prototype of the volatile inhalation anesthetics.
a. Halothane is a high-potency anesthetic.
b. Introduction of anesthesia is smooth and rapid.
c. Halothane is a weak analgesic, so coadministration of a strong analgesic is necessary.
d. Halothane has muscle relaxant properties, but the degree of relaxation produced is generally inadequate for surgery.
The volatile liquids that are used in inhalation anesthesia include:
Short-acting barbiturates (thiobarbiturates)
Short-acting barbiturates (thiobarbiturates) may be administered intravenously for induction of anesthesia. Thiobarbiturates have a rapid onset and short duration. Unconsciousness occurs in 10-20 seconds, and the patient will awaken in 10 minutes. There are two thiobarbiturates commonly used: thiopental sodium [Pentothal] and methohexital sodium [Brevital]
Benzodiazepines produce unconsciousness and amnesia when administered in large doses. Three benzodiazepines are administered IV: diazepam, lorazepam, and midozolam. Diazepam [Valium] induces unconsciousness in about 1 minute. Midazolam [Versed] may be used for induction of anesthesia and to produce conscious sedation.
Propofol [Diprivan] is an IV sedative-hypnotic used for induction and maintenance of anesthesia. Propofol has a rapid onset and a short duration of action. Adverse effects include respiratory depression and hypotension. Propofol poses a risk of bacterial infection because the drug is supplied in a mixture of soybean oil, glycerol, and egg lecithin. Pain at the IV site may also occur
Etomidate [Amidate] is a potent hypnotic used for induction of surgical anesthesia. The drug has no analgesic effects. The drug is preferred over barbiturates in patients with cardiovascular concerns
Ketamine [Ketalar] produces a state known as dissociative anesthesia in which the patient feels dissociated from his or her environment. Ketamine has a high potential for adverse psychological effects (such as hallucinations and delirium) and should therefore be avoided in patients with a history of psychiatric illness
Droperidol plus fentanyl
Droperidol plus fentanyl [Innovar] is a neuroleptic-opioid combination. It produces a unique state known as neurolept analgesia. Neurolept analgesia presents as sleep: the patient is quiet, indifferent, and insensitive to pain. Recent date show that droperidol prolongs the QT interval, indicating that it can cause potentially fatal dysrhythmias.
The three families of endogenous opioid peptides:
Three main classes of opioid receptors:
1) Mu receptors have the most pharmacological significance. Responses to mu receptors include analgesia, euphoria, respiratory depression, and sedation. In addition, mu activation is related to development of physical dependence. KO mice (Knock Off mice) in which mu receptors had been removed through genetic engineering failed to display analgesic effects or physical dependence in response to morphine
2) Kappa receptors can produce analgesia and sedation
3) Delta receptors do not have interactions with known opioids
Pure opioid agonists:
Pure opioid agonists activate mu receptors and kappa receptors. Pure opioid agonists can be either strong opioid agonists (morphine) or moderate to strong opioid agonists (codeine)
Agonist-antagonist opioids:
2) Agonist-antagonist opioids act on mu and kappa receptors. Whether they act as agonists or antagonists depends on the drug and which receptor it is acting on. When given alone, the agonist-antagonist opioids produce analgesia. When given in combination with a pure opioid agonist, agonist-antagonist opioids antagonize analgesia. The five agonist-antagonist opioids are:
a. Pentazocine – this is the prototype of the agonist-antagonist opioids
b. Nalbuphine
c. Butorphanol
d. Dezocine
e. Buprenorphine
Pure opioid antagonists:
Pure opioid antagonists act as antagonists at mu and kappa receptors. They do not produce analgesia or any of the other effects caused by opioid agonist. Their principle use is reversal of respiratory and CNS depression caused by overdose of opioid agonists
The structure of morphine is similar to:
the endogenous opioid peptide Met-Enkephalin.
The principle indication for morphine:
relief of moderate to severe pain
Adverse effects of morphine include:
Respiratory depression
Orthostatic hypotension
Urinary retention
Cough suppression
Biliary colic
Elevation of intracranial pressure
Adverse effects from prolonged use
Opioid overdose produces a classic triad of signs:
coma, respiratory depression, and pinpoint pupils.
Treatment for morphine (opioid) overdose:
Treatment is generally respiratory support and giving an opioid antagonist (naloxone).
Fentanyl is a strong opioid agonist that is available for parenteral, transdermal, and transmucosal administration. Fentanyl is about 100 times more potent than morphine.
1) Parenteral use of fentanyl is employed for induction and maintenance of surgical anesthesia
2) The transdermal patch is indicated for chronic severe pain
3) The transmucosal lozenge may be used for preanesthetic medication before surgery and for inducing conscious sedation prior to painful diagnostic or therapeutic procedures
Aside from morphine and fentanyl, strong opioid agonists include:
• Alfentanil and sufentanil are intravenous opioids related to fentanyl that are used for induction and maintenance of anesthesia
• Remifentanil is an intravenous opioid that is much more potent than morphine
• Meperidine shares the major pharmacologic properties of morphine
• Methadone has pharmacologic properties very similar to those of morphine
• Heroin is a strong opioid agonist that is very similar to morphine in structure and actions. It is an effective analgesic that is employed legally in Europe. Heroin has a greater lipid solubility than morphine, and it crosses the blood-brain barrier more easily. Once in the brain, heroin (diacetylmorphine) is rapidly converted into active metabolites: monoacetylmorphine (MAM) and morphine. MAM and morphine are responsible for the effects elicited by injection of heroin
• Hydromorphone, oxymorphone, and levorphanol are strong opioid agonists, similar to morphine, indicated for moderate to severe pain
The moderate to strong opioid agonists:
The moderate to strong opioid agonists are similar to morphine in terms of therapeutic and adverse effects. They cause analgesia, sedation, euphoria, respiratory depression, constipation, urinary retention, cough suppression, and miosis…they simply cause less of all those effects.
o Codeine is indicated for relief of mild to moderate pain. The drug is usually administered by mouth. Side effects are dose limiting. Codeine is an extremely effective cough suppressant.
o Oxycodone has analgesic actions equivalent to those of codeine. Controlled-release oxycodone [OxyContin] is a long-acting analgesic designed to relieve severe pain
o Hydrocodone
o Propoxyphene
1) Pentazocine is the prototype of the agonist-antagonist opioids. Pentazocine acts as an agonist at kappa receptors (to produce analgesia, sedation, and respiratory depression) and as an antagonist at mu receptors. Unlike the respiratory depression caused by morphine, respiratory depression caused by pentazocine is limited: beyond a certain dose, no further depression occurs. Pentazocine should never be administered to a patient who is physically dependent on a pure opioid agonist because it can precipitate an abstinence syndrome. Pentazocine can be given orally or parenterally
Nalbuphine and Butorphanol
Nalbuphine and Butorphanol have pharmacologic actions similar to pentazocine (they are agonist-antagonist opioids). They act as agonists at kappa receptors and as antagonists at mu receptors
Buprenorphine differs significantly from other opioid agonist-antagonists: the drug is a partial agonist at mu receptors and an antagonist at kappa receptors
Principle opioid antagonists include:
1) Naloxone [Narcan] is a structural analogue of morphine that acts as competitive antagonist on opioid receptors. Naloxone may be administered IV, IM, or SC. Therapeutic uses of naloxone include reversal of opioid overdose, reversal of postoperative opioid effects, and reversal of neonatal respiratory depression.
2) Naltrexone is a pure opioid antagonist that is approved for treating opioid abuse and alcohol abuse
3) Nalmefene is a long-acting analog of naltrexone that is approved for reversing postoperative opioid effects and treating opioid overdose
Nonopioid centrally acting analgesics:
Nonopioid centrally acting analgesics elieve pain by mechanisms largely unrelated to opioid receptors. These drugs include tramadol, clonidine, and ziconotide. These agents do not cause respiratory depression, dependence, or abuse, and are not regulated under the controlled substance act
Nociceptive pain
Nociceptive pain results from injury to tissues. Nociceptive pain can be either somatic pain (resulting from injury to somatic tissues such as bones, joints, and muscles) or visceral pain (resulting from injury to visceral organs such as the small intestine). Patients generally describe somatic pain as localized and sharp. Both forms of nociceptive pain respond well to opioid analgesics (morphine) as well as nonopioids (ibuprofen)
Neuropathic pain
Neuropathic pain results from injury to peripheral nerves. Neuropathic pain produces burning, shooting, jabbing, tearing, and numb sensations. Neuropathic pain responds poorly to opioids but well to adjuvant analgesics (antidepressants, local anesthetics, and anticonvulsants)
The WHO analgesic ladder with three steps based on intensity of pain:
1) Step 1 (mild to moderate pain) may be treated with a nonopioid analgesic, NSAIDS, and acetaminophen
2) Step 2 (more severe pain) adds opioid analgesics of moderate strength (oxycodone, hydrocodone)
3) Step 3 (severe pain) substitutes powerful opioids (morphine, fentanyl) for the weaker ones. For all cancer patients, pure opioid agonists are preferred to the agonist-antagonists.
Adjuvant analgesics:
analgesics are used to complement the effects of opioids and are therefore used in combination with opioids. Adjuvant analgesics include:
• Tricyclic antidepressants, such as Amitriptyline [Elavil], can enhance effects of opioids
• Anticonvulsants can relive neuropathic pain by suppressing spontaneous neuronal firing
• Local anesthetics/antidysrhythmics are second-line drugs for neuropathic pain
• CNS stimulants, such as dextroamphetamine [Dexedrine] and methylphenidate [Ritalin], enhance opioid-induced analgesia and counteract opioid-induced sedation
• Antihistamines, such as hydroxyzine [Vistaril], can reduce pain, anxiety, and nausea
• Glucocorticoids lack direct analgesic actions but can manage cancer-related conditions
• Bisphosphonates, such as etidronate [Didronel] and pamidronate [Aredia], can reduce cancer-related bone pain
Nondrug therapy for cancer pain may include:
Invasive therapies are the last resort for relieving pain. Examples of invasive therapies are
o Neurolytic nerve block (destroys neurons that transmit pain from a limited area)
o Radiation therapy (relieves pain by causing tumor regression)
o Neurosurgery (may destroy neurons that transmit pain, may implant opioid infusion systems, or may implant electrodes to stimulate neurons that release endogenous opioid peptides (endorphins)
o Tumor surgery
Physical interventions can help reduce pain, but their degree of pain relief is limited. Physical interventions include the application of heat and cold, massage, exercise, acupuncture, and transcutaneous electrical nerve stimulation
Psychosocial interventions can help patients cope by increase the sense of control over pain, reversing negative thoughts and feelings, and offering social support.
o Relaxation and imagery (meditation, music) induce mental relaxation and physical relaxation
o Cognitive distraction (prayer) diverts attention away from pain and negative emotions
o Peer support groups provide emotional support
Cluster headaches
Cluster headaches occur in a series of attacks and may be separated for month-long to year-long attack-free intervals. Primary therapy of cluster headaches is directed at prophylaxis.Cluster headaches are marked by unilateral pain in the inner eye
Tension headaches
2) Tension headaches are the most common type of headache. Nonthrobbing pain occurs in a headband distribution. Tension headaches may be episodic or chronic, but they occur 15 or more days per month for at least 6 months. An acute attack of mild to moderate severity can be relieved with a nonopioid analgesic. A tricyclic antidepressant (amitriptyline) is used for prophylaxis. In addition to receiving drugs, patients should be taught how to manage stress.
Possible triggers for migraines include:
o Emotions (stress, anticipation, anxiety, depression, excitement, frustration)
o Foods that contain monosodium glutamate, tyramine, nitrates, phenylethylamine (chocolate), aspartame
o Drugs such as alcohol, analgesics, caffeine, cimetidine, cocaine, estrogens, nitroglycerin
o Other causes such as carbon monoxide, hormonal changes in women, flickering lights/glare, loud noises, change in altitude or barometric pressure, birth control, magnesium levels, altered sleep pattern
Calcitonin gene-related peptide:
CGRP promotes migraine.Data that implicate CGRP as a cause of migraine include:
• Plasma levels of CGRP rise during migraine
• Stimulation of neurons of the trigeminal vascular system promotes release of CGRP
• CGRP is a potent vasodilator
The role of 5HT in migraine:
Serotonin prevents migraine.Data that support a suppressive role for serotonin include:
• 5HT levels drop by 50% during a migraine attack
• Depletion of 5HT can trigger an attack in migraine-prone individuals
• Administration of serotonin can abort an ongoing attack
Ophthalmoplegic migraine:
Ophthalmoplegic migraine is characterized by pain behind one eye. This type of migraine causes less pain than a standard migraine. Paralysis of eye muscles, double vision, and droopy eyelid also occurs.
Retinal migraine:
Retinal migraine is characterized by short-term blind spots or total blindness in one eye, with or without an accompanying headache
Familial hemiplegic migraine:
Familial hemiplegic migraine is a very rare, inherited migraine. If both parents suffer from it, the offspring has a 75% chance of suffering too. If one parent suffers from it, the offspring has a 50% chance of suffering too. Familial hemiplegic migraine usually begins in childhood (as early as 1-2 years) and generally ceases as the child grows older. Symptoms include hemiplegia (paralysis on one side of the body), fever, vision problems, and vertigo
Analgesics for migraine:
a. Aspirin-like analgesics such as NSAIDs and acetaminophen can provide adequate relief of mild to moderate symptoms.
b. Opioid analgesics such as Demerol and Stadol are powerful drugs reserved for severe migraine that has not responded to first-line medication.
Ergot alkaloids:
Ergot alkaloids, such as ergomar, are used to treat moderate to severe migraine symptoms
Serotonin 1B/1D-receptor agonists:
Serotonin 1B/1D-receptor agonists (triptans) such as sumatriptan [Imitrex], are first-line drugs for migraines. They relieve pain by constricting intracranial blood vessels and suppressing the release of inflammatory neuropeptides. Adverse effects include chest symptoms, coronary vasospasms, and teratogenesis
Prophylactic therapy for migraine headache:
Beta blockers
Calcium channel blockers
Tricylic antidepressants
Drugs for managing RA fall into three major classes:
1. Nonsteroidal anti-inflammatory drugs
2. Disease-modifying antirheumatic drugs
3. Glucocorticoids
Methotrexate [Rheumatrex] is the most rapid-acting DMARD. Therapeutic effects may develop in 3-6 weeks. Methotrexate is an anticancer drug that inhibits folic acid synthesis. Major toxicities are hepatic fibrosis, bone marrow suppression, GI ulceration, and pneumonitis.
Etanercepto [Enbrel] is a newer DMARD that binds tightly to tumor necrosis factor (TNF) receptors on cells, thereby preventing TNF from interacting with its normal receptors. It is used for moderate to severe RA. The drug is very expesive: $14,000-37,000 per year. Adverse effects include an increased risk of infection and injection site reactions
Infliximab [Remicade] is a TNF antibody that blocks TNF receptors. IT is used for RA and Crohn’s disease
Adalimumab [Humira] is DMARD that is a monoclonal antibody that binds to and neutralizes TNF
Anakinra [Kineret] is a DMARD that blocks receptors for interleukin-1
Colchine is an anti-inflammatory agent whose effects are specific for gout. It can treat an acute gouty attack, reduce the incidence of attacks, and abort an impending attack. Colchicine inhibits leukocyte migration and infiltration. The most characteristic signs of colchicine toxicity are nausea, vomiting, diarrhea, and abdominal pain.
Indomethacin [Indocin] is a first-choice NSAID used to treat acute gouty arthritis. Indomethacin causes minimal GI side effects, but it may cause severe frontal headache.
Allopurinol [Zyloprim] reduces blood levels of uric acid. It does so by inhibiting reabsorption of uric acid in renal tubules. It is used for chronic, tophaceous gout and hyperuricemia due to chemotherapy. The figure shows the reduction of uric acid formation by allopurinol. Allopurinol is generally well-tolerated. Adverse effects include hypersensitivity syndrome, characterized by rash, fever, and dysfunction of the kidneys/liver. (rare but serious). Mild effects include GI disturbance and neurologic effects (drowsiness, headache, cataracts).
Probenecid [Benemid] acts on renal tubules to inhibit reabsorption of uric acid
Sulfinpyrazone [Anturane] is used to reduce hyperuricemia in patients with chronic gout
Natural immunity:
Natural immunity is innate and consists of factors present prior to exposure to an infectious agent. Examples of natural immunity include physical barriers such as skin, phagocytic cells, and natural killer cells. All responses of natural immunity are nonspecific.
Specific acquired immunity:
Specific acquired immunity is created only after exposure to a foreign substance called an antigen. With each succeeding re-exposure to a particular antigen, the specific immune response becomes more rapid and more intense. There are two types of specific acquired immunity:
a. Cell mediated immunity refers to immune responses in which targets are attacked directly by immune system cells, specifically, cytolytic T cells and macrophages
b. Humoral immunity refers to immune responses that are mediated by antibodies
B lymphyocytes:
B lymphyocytes (B cells) have the job of making antibodies. Hence, B cells mediate humoral immunity. B cells circulate in both the blood and lymph and they are produced in the bone marrow
Cytolytic T lymphocytes:
Cytolytic T lymphocytes (Cytolytic T cells, CD8 cells) attack and kill target cells directly. Specificity of the attack is determined by the by presence of antigen molecules on the surface of the target cell and specific receptors for that antigen on the surface of the T cells. T cells circulate in both the blood and lymph and they are produced in the thymus gland
Helper T lymphocytes:
Helper T lymphocytes (Helper T cells, CD4 cells) contribute to the immune response in three ways:
1. They have an essential role in antibody production by B cells
2. They release factors that promote delayed-type hypersensitivity (DTH)
3. They participate in the activation of cytolytic T cells
Helper T cells are the immune cells that HIV attacks; because of helper T-cell loss, AIDS patients are at a high risk of death from opportunistic infections
Macrophages are produced in the bone marrow, enter the blood as monocytes, and then infiltrate tissues, where they evolve into macrophages. Macrophages are present in all organs and tissues. The primary function of macrophages is phagocytosis. They also are required for activation of T cells (when performing this function, they are referred to as antigen presenting cells), they are the final mediators of DTH, and they phagocytize cells that have been tagged with antibodies.
Dendritic cells:
Dendritic cells are found in the lymph. They perform the same antigen-presenting tasks as macrophages, but they do not serve as scavengers
Mast cells:
Mast cells, which are derived from basophils, are concentrated in the skin and other soft tissues. Mast cells mediate immediate hypersensitivity reactions
Basophils are the precursors of mast cells and are found in the blood. Basophils mediate hypersensitivity reactions
Neutrophils(polymorphonuclear leukocytes) phagocytize bacteria and other foreign particles. Neutrophils avidly devour cells that have been tagged with antibodies of IgG, so they are important effectors of humoral immunity
Eosinophils attack and destroy foreign particles that have been coated with antibodies of the IgE class. Their usual target is helmiths (parasitic worms). Eosinophils contribute to tissue injury and inflammation associated with immediate hypersensitivity reactions.
Located in mucous membranes of the GI tract and lungs and in many secretions, IgA serves as a first line of defense against microbes.

IgA is transferred to infants via breast milk.
Found only on the surface of mature B cells, where it serves as a receptor for antigen recognition (along with IgM)
Binds to the surface of mast cells; subsequent binding of antigen to IgE stimulates the release of histamine, heparin, and other mediators form the mast cells.

Binds to parasitic worms
IgG is the major antibody in the blood. It fixes complement, enhances phagocytosis, and is transferred across the placenta to the fetal circulation where it provides neonatal immunity.
Vaccination is a term that refers to administration of any vaccine or toxoid (vaccination refers only to the production of active immunity).
Cytolytic T lymphocytes:
Cytolytic T lymphocytes are a branch of cell-mediated immunity that kill other virally infected cells. Activation of cytolytic T cells requires the participation of an APC and a CD4 cell. CTLs recognize their targets by the presence of an antigen-MHC I complex
Delayed-type hypersensitivity:
DTH is a type of cell-mediated immunity. It is a mechanism that tries to rid the body of bacteria that replicate within macrophages. For DTH to occur, both an infected macrophage and a CD4 helper T cell are needed. The macrophage serves to activate the CD4 cell, which in turn activates the macrophage to kill the bacteria residing in it. Interferon-gamma, released from the CD4 cell, is the major stimulus for macrophage activation.
Antibody-mediated (humoral) immunity:
Antibody production requires the interaction of three types of cells: B cells, which actually make the antibodies; helper T cells (CD4+ cells), which stimulate the B cells; and an antigen-presenting cell (macrophage or dendritic cell), which activates the CD4 cells so they can help the B cells.
Specific immune responses can be viewed as having three main phases:
1) Recognition phase occurs when a mature lymphocyte (B or T cell) encounters its matching antigen.
2) Activation phase occurs when antigen recognition causes the lymphocyte to become activated and undergo proliferation and differentiation. Some of the daughter cells actively participate in the immune responses, while other daughter cells differentiate into memory cells
3) Effector phase in which the immune system attempts to eliminate the specific antigen that initiated the response. With cell-mediated immunity, antigen-bearing cells can be lysed by cytolytic T cells, or they can be ingested by macrophages. In antibody-mediated immunity, target cells may be primed for attacked by phagocytes or by the complement system.
IgM is the first class of antibody produced in response to an antigen. It, along with IgD, serves as a receptor on the surface of B cells.
Cytokine is a term that refers to any mediator molecule (other than an antibody) that is released by immune cells. A lymphokine is a cytokine released by a lymphocyte, and monokine is a cytokine released by a mononuclear phagocyte (monocyte or macrophage)
Cell-mediated immunity and humoral immunity share five characteristic features:
1) Specificity. Cell-mediated and humoral immunity are triggered by specific antigens, and their purpose is to destroy the antigen that triggered the response in the antigen response because of specific receptors on B and T cells
2) Diversity. Our immune system can respond to millions of different antigens
3) Memory. Exposure to an antigen affects the immune system such that re-exposure produces a faster, larger, and more prolonged response
4) Time limitation. Immune responses don’t last indefinitely
5) Selectivity for antigens of non-self origin. Our immune system targets only foreign antigens. This discrimination between self and non-self is made possible by major histocompatibility complex (MHC) molecules. The MHC is a group of genes that codes for MHC molecules to be expressed on the surface of all cells. When the ability to discriminate between self and non-self fails, our immune systems can attack our own cells (autoimmune diseases).
Immunization refers to production of both active and passive immunity. The purpose of immunization is to protect against infectious diseases.
Active immunity:
Active immunity is the long-lasting endogenous production of antibodies.
Passive immunity:
Passive immunity is conferred by giving a patient preformed antibodies (specific immune globulins) to create an immediate but short-lived response.
National Childhood Vaccine Act of 1986:
The National Childhood Vaccine Act of 1986 requires a permanent record of each mandated vaccination a child receives. The following data are required:
Date of vaccination
Route and site of vaccination
Vaccine type, manufacturer, lot number, and expiration date
Name, address, and title of the person administering the vaccine
Adverse reaction to DTP:
Acute encephalopathy
Adverse reaction to MMR:
Thimersol, a mercury-based preservative found in vaccines, may be linked to autism
Target diseases for routine childhood vaccination include:
Measles, mumps, and rubella
Diphtheria, tetanus, and pertussis
Hepatitis B virus
Hepatitis A virus
Pneumococcal infections
Influenza virus
Varicella virus
Types of immunosuppresants:
1) Calcineurin inhibitors
2) Glucocorticoids
3) Cytotoxic drugs
4) Antibodies
Calcineurin inhibitors:
Calcineurin inhibitors such as cyclosporine, tacrolimus, and sirolimus are the most effective immunosuppressants available. These drugs inhibit calcineurin and thereby suppress production of interleukin-2 (calcineurin promotes synthesis of cytokines). The principle use of these drugs is prevention of organ rejection in transplant recipients.
Cyclosporine [Sandimmune] is a powerful immunosuppressant. It suppresses the production of interleukin-2 and is used to prevent rejection of organs in transplant patients but also may be used for some autoimmune diseases. Adverse effects of cyclosporine include nephrotoxicity, increased risk of infection, hepatotoxicity, lymphomas, hypertension (10-15% increase develops in 50% patients), embryotoxicity, and anaphylactic reactions. Drugs that can decrease cyclosporine levels include drugs that can induce hepatic microsomal enzymes. Drugs that can increase cyclosporine levels include antifungal drugs, macrolide antibiotics, and amphotericin B. Rental damage may be intensified by concurrent use of other nephrotoxic drugs. Grapefruit juice can increase cyclosporine levels by 50-200%
Tacrolimus [Prograf] is an alternative to cyclosporine for prophylaxis of organ rejection. At this time, it is approved only for liver transplants. Adverse effects include nephrotoxicity (the major concern), neurotoxicity, GI effects, hypertension, and hyperkalemia. Agents that inhibit CYP3A (an isozyme of cytochrome P450) and grapefruit juice may increase tacrolimus levels. NSAIDs can injure the kidneys and should be avoided.
Sirolimus [Rapamune] is an immunosuppressant approved for prevention of renal transplant rejection. The drug should be used in conjunction with cyclosporine and glucocorticoids. Adverse effects include increased risk of infection, high levels of cholesterol and triglycerides, risk of renal injury, and severe complications in the liver and lung. Drugs that inhibit or induce CYP3A4 (the 3A4 isozyme of cytochrome P450), high-fat foods, and grapefruit juice can all cause sirolimus levels to increase
Glucocorticoids in immunosuppression:
Glucocorticoids such as prednisone are used widely to suppress immune responses. Immunosuppressant applications range from suppression of transplant rejection to treatment of asthma to therapy of autoimmune disorders
Cytotoxic drugs in immunosuppresion:
Cytotoxic drugs suppress immune responses by killing B and T lymphocytes that are undergoing proliferation. These drugs are nonspecific, so they are toxic to all proliferating cells.
Azathioprine [Imuran] is a cytotoxic drug that suppresses cell-mediated and humoral immune responses. It is employed to as an adjunct to suppress rejection of renal transplants. It is also used for various autoimmune disorders. Adverse effects include neutropenia (decreased number of neutrophils), thrombocytopenia (decreased number of platelets), and neoplasms (brain tumors).
Used as an immunosuppresant, Muromonab-CD3 is a monoclonal antibody that binds to the CD3 site on human T lymphocytes. Upon binding, the antibody blocks all T-cell functions. The drug is used to prevent rejection of transplants and to deplete T cells from bone marrow prior to bone marrow transplant. Adverse effects include fever, chills, dyspnea, chest pain, and N/V.
Basiliximab and Daclizumab:
Used as immunosuppressants, Basiliximab and Daclizumab are monoclonal antibodies that bind to the receptor for IL-2 on T lymphocytes. As a result, these antibodies block activation of T cells by IL-2. They are used for prophylaxis of acute organ rejection following a renal transplant.
Antibodies directed at the components of the immune system include:
Basiliximab and Daclizumab
Lymphocyte immune globulin
Antithymocyte globulin
Rho(D) immune globulin
H1 receptor:
Activation of H1 receptors causes dilation of small blood vessels, increased capillary permeability, bronchoconstriction, itching, pain, secretion of mucus, and neurotransmitter effects in the CNS
H2 receptor:
The major response to activation of H2 receptors is secretion of gastric acid
Second generation H1 receptor antagonists:
Second generation H1 receptor antagonists are generally nonsedating. Common second generation H1 antagonists include:
a. Fexofenadine [Allegra]
b. Cetirizine [Zyrtec]
c. Loratadine [Claritin, Tavist ND, Alavert]
d. Desloratadine [Clarinex]
e. Azelastine [Astelin]
First generation H1 receptor antagonists:
First generation H1 receptor antagonists produce selective blockade of H1 receptors. All first generation H1 antagonists are known to cause sedation and muscarinic blockade (dry mouth, urinary hesitancy) to varying degrees. The principle use of H1 blockers is treatment of mild allergic disorders, though they may also be used for severe allergy, motion sickness, insomnia, and the common cold.

Adverse effects of H1 antagonists include sedation, nonsedative CNS effects (like dizziness, incoordination, confusion, and fatigue), GI effects, anticholinergic effects (such as dry mouth and drying of mucus in the nasal passageways and throat), and cardiac dysrhythmias.

Common first generation (sedating) H1 antagonists include:
a. Alkylamines such as chlorpheniramine and brompheniramine [Dimetapp]
b. Ethanolamines such as diphenhydramine
c. Phenothiazines such as promethazine
d. Piperazines such as hydroxyzine
e. Piperidines such as azatadine

Motion sickness may be treated with promethazine [Phenergan] or dimenhydrinate [Dramamine], both of which block H1 receptors and muscarinic receptors in the neuronal pathway leading from the vestibular apparatus of the inner ear to the vomiting center of the medulla
The cyclooxygenase inhibitors fall into two major categories:
1) Drugs that have anti-inflammatory properties (NSAIDs)
a. First generation (aspirin) inhibits COX-1 and COX-2.
b. Second generation (celecoxib) inhibits COX-2 only
2) Drugs that lack anti-inflammatory properties (acetaminophen)
Adverse effects of aspirin include:
• Gastrointestinal effects such as gastric distress, heartburn, and nausea
• Bleeding due to inhibition of platelet aggregation
• Renal impairment, which is signaled by reduced urine output
• Salicylism is a syndrome that begins to develop when aspirin levels climb over therapeutic levels. Signs of salicylism include tinnitus (ringing in ears), sweating, headache, dizziness, and development of acid-base imbalance in plasma
• Reye’s syndrome is a rare but serious illness of childhood that is characterized by encephalopathy and fatty liver degeneration. Aspirin should be avoided by children that have influenza or chickenpox to prevent the development of Reye’s syndrome
• There may be a risk to the developing fetus because aspirin is able to cross the placenta
• Hypersensitivity reactions develop in rare cases. They resemble anaphylaxis, but they are not mediated by the immune system
First generation NSAIDs include:
Aspirin (Irreversible inhibitor)
Ibuprofen (Propionic acid derivative)
Naproxen (Propionic acid derivative)
The principle indications for the nonaspirin NSAIDs:
Rheumatoid arthritis and osteoarthritis
Celecoxib [Celebrex] is a second generation cyclooxygenase inhibitor that is selective for COX-2.
It causes fewer adverse effects than first generation NSAIDs.
Celecoxib is indicated for osteoarthritis, rheumatoid arthritis, acute pain, dysmenorrheal, and familial adenomatous polyposis (inherited colorectal cancer).
Celecoxib does not provide the cardiovascular benefits of aspirin because it does not inhibit COX-1 in platelets to suppress platelet aggregation
Adverse effects of celecoxib include dyspepsia (ulcers), abdominal pain, renal toxicity, and precipitation of an allergic reaction in patients allergic to sulfonamides.
Rofecoxib [Vioxx] and Valdecoxib [Bextra]:
Rofecoxib [Vioxx] and Valdecoxib [Bextra] are newer second generation cyclooxygenase inhibitors. They also produce selective inhibition of COX-2. However, the Vioxx GI Outcomes Research (VIGOR) conducted in 2000 indicated that in high doses, the drugs may cause cardiovascular events, myocardial infarction, and stroke.
Acetaminophen (Tylenol) has analgesic and antipyretic activities similar to aspirin, but it is devoid of clinically useful anti-inflammatory and antirheumatic actions. Whereas aspirin can inhibit synthesis of prostaglandins in both the CNS and the periphery, inhibition by acetaminophen is limited to the CNS.
The most common adverse effect is hepatotoxicity (the principle feature of overdose is hepatic necrosis). Liver damage can be minimized by giving acetylcysteine [Mucomyst], a specific antidote to acetaminophen.
Acetylcysteine reduces injury by substituting for depleted glutathione in the reaction that converts the toxic metabolite of acetaminophen to its nontoxic form. The metabolism of acetaminophen is shown in the figure. The liver is unable to convert toxic metabolites to the nontoxic form in chronic alcoholics
When glucocorticoids are used to treat nonendocrine disorders, physiologic responses occur as a side effect. These include:
• Metabolic effects. Glucocorticoids influence the metabolism of carbohydrates, proteins, and fats. They stimulate lipolysis (fat breakdown) and can cause fat redistribution with long-term use.
• Cardiovascular effects. Glucocorticoids are required to maintain the functional integrity of the vascular system
• Effects during stress. At times of stress, the adrenals secrete large quantities of glucocorticoids and epinephrine to help maintain blood pressure and plasma levels of glucose
• Effects on water and electrolytes. Glucocorticoids can exert actions like those of aldosterone
• Respiratory system in neonates. Glucocorticoids hasten maturity of the lungs
In nonendocrine disorders, therapeutic uses of glucocorticoids include:
• Rheumatoid arthritis
• Systemic lupus erythematosus
• Inflammatory bowel disease
• Miscellaneous inflammatory disorders
• Allergic conditions
• Asthma
• Dermatologic disorders
• Neoplasms
• Suppression of allograft rejection
• Prevention of respiratory distress syndrome in preterm infants
Adverse effects of glucocorticoids include:
o Adrenal insufficiency
o Osteoporosis
o Infection
o Glucose intolerance
o Myopathy
o Fluid and electrolyte disturbance
o Growth retardation
o Psychologic disturbances
o Cataracts and glaucoma
o Peptic ulcer disease
o Iatrogenic Cushing’s syndrome
Therapeutic uses of cortisone:
Cortisone is a glucocorticoid that is primarily used for anti-inflammatory purposes. Immunosuppressive actions such as:
• Inhibition of the synthesis of chemical mediators
• Suppression of the infiltration of phagocytes
• Suppression of lymphocyte proliferation
• Suppression of protein synthesis
Stroke volume is determined by three factors:
1) Myocardial contractility (the force at which the ventricles contract)
2) Afterload (the load against which a muscle exerts its force – i.e. the arterial pressure that the left ventricle must overcome to eject blood)
3) Cardiac preload (the amount of tension/stretch applied to a muscle prior to contraction – i.e. the force of venous return: the greater the filling pressure, the greater the ventricles will stretch)
Starling’s Law of the heart:
Starling’s Law of the heart states that the force of ventricular contraction is proportional to muscle fiber length. When more blood enters the heart, more blood is pumped out. Increased SV leads to increased CO.
Venous return is the primary determinant of SV and CO. Factors that determine venous return include:
• Systemic filling pressure is the most important factor. This is the force at which blood is returned to the heart
• Auxiliary muscle pumps (skeletal muscle and respiratory)
• Resistance to flow between peripheral vessels and the right atrium
• Right atrial pressure
Angiotensin II:
Angiotensin II mediates essentially all of the effects of the RAAS. The most prominent effects are vasoconstriction and aldosterone release from the adrenal cortex
Aldosterone acts on the kidney to cause retention of sodium and excretion of potassium and hydrogen. Because retention of sodium causes water to be retained too, aldosterone increases plasma volume, and thereby increases blood pressure.
Prototype of the ACE inhibitors
Therapeutic uses of ACE inhibitors include:
Therapeutic uses of ACE inhibitors include heart failure; acute MI; left ventricular dysfunction; diabetic and nondiabetic nephropathy; and prevention of MI, stroke, and death in patients at high cardiovascular risk. Beneficial effects of ACE inhibitors derive from 1) reducing levels of angiotensin II and 2) increasing levels of bradykinin (which promotes vasodilation).
Adverse effects of ACE inhibitors:
• First-dose hypotension (a precipitous drop in BP following the first dose of an ACE inhibitor)
• Fetal injury (use during the second and third trimesters may cause harm to the developing fetus)
• Cough (persistent, dry, irritating, and nonproductive cough is common)
• Angioedema (a rare but fatal reaction to the accumulation of bradykinin caused by ACE inhibitors)
• Hyperkalemia (potassium accumulation may occur if the patient is taking a potassium supplement)
• Dysgeusia (impaired or distorted sense of taste) and rash
• Renal failure (severe renal insufficiency can occur in patients with bilateral renal artery stenosis or stenosis in the artery to a single remaining kidney)
• Neutropenia (rare but serious, causes risk of infection)
Drug interactions with captopril include:
o Diuretics (may intensify first-dose hypotension)
o Antihypertensive agents (have an additive effect with ACE inhibitors)
o Drugs that raise potassium levels (increase the risk of hyperkalemia)
o Lithium (ACE inhibitors can make lithium accumulate to toxic levels)
Prototype of the angiotensin II receptor blockers
Angiotensin II receptor blockers:
Angiotensin II receptor blockers decrease the influence of angiotensin II by blocking the actions of angiotension II (whereas ACE inhibitors block angiotensin II production). ARBs cause dilation of arterioles and veins and prevent angiotensin II from inducing pathologic changes in cardiac structure. By blocking angiotensin II receptors in the adrenals, ARBs decrease release of aldosterone, and can thereby increase renal excretion of sodium and water and reduce excretion of potassium. In contrast to ACE inhibitors, ARBS do not increase levels of bradykindin (because they do not inhibit kinase II). This means that they do not promote cough like ACE inhibitors do.
Therapeutic uses of ARBS include:
1. Hypertension
2. Heart failure
3. Diabetic nephropathy
4. Losartan may also be used for treatment of MI, migraine headache, and prevention of strokes.
Spironolactone is a selective aldosterone receptor blocker, but it is less selective than eplerenone and may bind with receptors for other steroid hormones too. Spironolactone may be used to treat hypertension and heart failure. Adverse effects include hyperkalemia, gynecomastia, menstrual irregularities, impotence, hirsutism, and deepening of the voice
Eplerenone is a selective aldosterone receptor blocker. The greatest risk with eplerenone is hyperkalemia, so the patient must avoid potassium supplements, salt substitutes, or potassium-sparing diuretics.
Drug interactions with eplerenone include
• Inhibitors of CYP3A4 (can increase levels of eplerenone and pose risk of toxicity)
• Drugs that raise potassium levels (can increase the risk of hyperkalemia)
• Lithium (eplerenone can raise lithium levels)
Selective aldosterone receptor blockers:
Selective aldosterone receptor blockers cause selective blockade of aldosterone receptors, having little or no effect on receptors for other steroid hormones. They may be used to treat hypertension and heart failure. These drugs should be reserved for patients who have not responded to traditional antihypertensive drugs.
The three families of calcium channel blockers:
1) Dihydropyridines (nifedipine)
2) Phenylalkylamine (verapamil)
3) Benzothiazepine (diltiazem)

The dihydropyridines act primarily on arterioles; in contrast, verapamil and diltiazem act on arterioles and on the heart.
Verapamil belongs to the phenylalkylamine family of CCBs. It blocks calcium channels in blood vessels and heart. The overall hemodynamic response to verapamil is the net result of 1) direct effects on blood vessel and 2) reflex responses.

Direct effects of verapamil include vasodilation, reduced arterial pressure, increased coronary perfusion, reduced heart rate via blockade of SA node, decreased AV nodal conduction via blockade of AV node, decreased force of myocardial contraction
Indirect (reflex) effects include verapamil-induced lowering of blood pressure activates the baroreceptor reflex, causing increased firing of sympathetic nerves to the heart. Since these indirect effects are counterbalanced by the direct effects, the drug has little net effect on cardiac performance.
Therapeutic uses of verapamil include:
• Angina pectoris (benefits are derived from vasodilation)
• Essential hypertension (benefits are derived from vasodilation)
• Cardiac dysrhythmias (verapamil slows ventricular rate)
• Migraine headache
Adverse effects to verapamil include:
Adverse effects include constipation (resulting from blockade of calcium channels in the smooth muscle of the intestine), dizziness, facial flushing, headache, and edema of the ankles and feet (all of which occur secondary to vasodilation). Gingival hyperplasia (overgrowth of gum tissues) may also develop.
The prototype of the dihydrophyridines
Dihydropyridines are agents that act mainly on vascular smooth muscle. Dihydropyridines cause vasodilation by blocking calcium channels. The net effect of their direct and indirect effects is:
1) Lowered blood pressure (increased coronary perfusion)
2) Increased heart rate (baroreceptor reflex)
3) Increase contractile force (baroreceptor reflex)

Therapeutic uses of dihydropyridines include angina pectoris, hypertension, and it has been used on an investigational basis to suppress preterm labor
Adverse effects related to vasodilation include:
1) Postural/orthostatic hypotension (vasodilation in veins)
2) Reflex tachycardia
3) Expansion of blood volume may occur by two mechanisms
a. The RAAS senses a decrease in BP and triggers aldosterone secretion
b. The kidneys to reabsorbs an increased fraction of filtered sodium and water, which causes blood volume to expand.
Hydralazine is a vasodilator that causes selective dilation of arterioles. The drug has little or no effect on veins. The mechanism of action is unknown. Since hydralazine acts selectively on arterioles, postural hypotension is minimal.
Therapeutic uses of hydralazine include essential hypertension (for which a beta blocker and diuretics are also used), hypertensive crisis, and heart failure
Adverse effects include reflex tachycardia, increased blood volume, and systemic lupus erythematosus-like syndrome
Hydralazine is combined with a beta blocker to protect against reflex tachycardia, and with diuretics to prevent sodium and water retention. Drugs that lower BP will intensify hypotensive responses to hydralazine.
Minoxidil produces more intense vasodilation than hydralazine, but also causes more serous adverse reactions so it is generally reserved for severe hypertension. Minoxidil causes selective dilation of arterioles. It is rapidly absorbed and extensively metabolized to minoxidil sulfate.
Vasodilation by minoxidil results from a direct action on vascular smooth muscle: once minoxidil is metabolized to minoxidil sulfate, the metabolite causes potassium channels in the VSM to open, thus hyperpolarizing the VSM cells so they cannot contract.
To minimize adverse cardiovascular responses, minoxidil should be used with a beta blocker plus intensive diuretic therapy. Topical minoxidil [Rogaine] is used to promote hair growth in balding men.
Adverse effects of minoxidil include reflex tachycardia, sodium and water retention, hypertrichosis (excessive growth of hair), and pericardial effusion (a rare accumulation of fluid beneath the pericardium)
Sodium nitroprusside:
Sodium nitroprusside is a potent and fast-acting antihypertensive agent. It causes venous and arteriolar dilation. Administration is by IV infusion, and the onset of effects is immediate.
Niroprusside is used to lower blood pressure during hypertensive emergencies. Adverse effects include excessive hypotension, cyanide poisoning (in patients with liver disease), and thiocyanate (a metabolite) toxicity
Vasodilators OTHER than hydralazine, minoxidil, and sodium nitroprusside:
• Angiotensin-converting enzyme inhibitors
• Angiotensin II receptor antagonists
• Organic nitrates such as nitroglycerin (promotes dilation of the veins)
• Calcium channel blockers (dilates the arterioles)
• Sympatholytics (prevents the sympathetic nervous system from causing vasoconstriction)
11 principle sites at which antihypertensive drugs may act:
1) Brainstem = suppresses sympathetic outflow to the heart and blood vessels
2) Sympathetic ganglia = reduces sympathetic stimulation of heart and blood vessels
3) Terminals of adrenergic nerves = decrease the release of NE
4) Beta1-adrenergic receptors on the heart = prevents sympathetic heart stimulation
5) Alpha1-adrenergic receptors on blood vessels = promotes dilation of arteries and veins
6) Vascular smooth muscle = causes relaxation
7) Renal tubules = promotes sodium and water excretion
8) Beta1 receptors on juxtaglomerular cells = suppresses renin release
9) Angiotensin-converting enzyme = suppress formation of angiotensin II
10) Angiotensin II receptors = prevents the actions of angiotensin II
11) Aldosterone receptor blockade = promotes sodium and water excretion
Diuretics are vasodilators which many cause the adverse effects hypokalemia, dehydration, hyperglycemia, and hyperuricemia, have three main types:
• Thiazide diuretics – causes reduction of blood volume and arterial resistance
• High-ceiling (loop) diuretics – produces a much greater loss of fluid than thiazide diuretics
• Potassium-sparing diuretics – produces a smaller amount of fluid loss
Sympatholytics are vasodilators that suppress the influence of the sympathetic nervous system on the heart, blood vessels, and other structures. There are five subcategories of sympatholytic drugs:
• Beta-adrenergic blockers decrease HR, CO, suppress reflex tachycardia, reduce release of renin, and reduce peripheral vascular resistance
• Alpha1 blockers suppress stimulation of alpha1 receptors on arterioles and veins to prevent vasoconstriction
• Alpha/beta blockers (carvedilol and labetalol) are able to block both beta1 and alpha1 receptors.
• Centrally acting alpha2 agonists act within the brainstem to suppress sympathetic outflow to the heart and blood vessels
• Adrenergic neuron blockers decrease blood pressure through actions in the terminals of postganglionic sympathetic neurons
Direct-acting vasodilators:
Direct-acting vasodilators such as hydralazine or minoxidil reduce blood pressure through vasodilation of arterioles
Classes of antihypertensive drugs:
Direct-acting vasodilators
Calcium channel blockers
ACE inhibitors
Angiotensin II receptor blockers
Aldosterone antagonists
Hypertensive emergencies:
A hypertensive emergency exists when diastolic blood pressure exceeds 120 mm Hg. The major drugs for hypertensive emergency, all of which are administered by IV, include:
o Sodium nitroprusside
o Fenoldopam [Corlopam]
o Labetalol [Trandate]
o Diazoxide [Hyperstat IV]
Drugs for heart failure:
Drugs that inhibit RAAS
Beta blockers
Inotropic agents
Inotropic agents:
Inotropic agents are drugs that increase the force of myocardial contraction. They are given to improve performance of the failing heart. Three types of inotropic agents are available:
1) Cardiac glycosides reduce symptoms but do not prolong life. They are naturally occurring compounds from the Digitalis plant (foxglove) that inhibit the Na+/K+ pump so that more Ca++ can enter the cell = increased contractility.
2) Sympathomimetics such as the catecholamines dopamine [Intropin] and dobutamine [Dobutrex] can activate beta1-adrenergic receptors on the heart to increases heart rate, dilate renal blood vessels, and activate alpha1 receptors in blood vessels (activating alpha1 receptors increases vascular resistance and reduces CO)
3) Phosphodiesterase inhibitors such as inamrinone and milrinone increase myocardial contractility and promote vasodilation. This occurs because inhibition of phosphodiesterases causes intracellular accumulation of cAMP
Digoxin is a cardiac glycoside indicated for heart failure and dysrhythmias. Digoxin exerts a positive inotropic action on the heart. That is, the drug actually increases the force of ventricular contraction, and thereby increases CO. Hypokalemia secondary to the use of diuretics is the most common cause of dysrhythmias in patients receiving digoxin