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95 Cards in this Set
- Front
- Back
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Properties of Anesthesia
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-Unconsciousness
-Amnesia -Blunting of protective reflexes -Reduced muscle tone |
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Isoflurane, Sevoflurane, Desflurane, Enflurane, Halothane, NO
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Inhaled anesthetics; administered via inspired gas and eliminated via expired gas; volatile liquids at room T (except NO gas at room T)
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Thiopental, Methohexital, Etmidate, Propofol, Ketamine
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Intravenous anasthetics
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Stages 1-4 of Anesthesia
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Stage 1: Analgesia; if use NO or ketamine, will also have increase in pain tolerance; reflexes still intact
Stage 2: Excitement/Disinhibiton-Thrashing without stimulation, patient unresponsive; try to get through this stage as fast as possible -Stage 3: Surgical anesthesia-do not move in response to surgical incision -Stage 4: Medullary depression-do not want to be in this stage because of cardiovascular and respiratory depression |
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Why are Enflurane and Holathane no longer used as inhaled anasthetics?
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-They have the highest B/G ratio, meaning that too much of the drug is dissolved in the blood
-Because of their high solubility, it takes them too long to kick in and it takes to long for the patient to emerge -metabolized more than the other drugs, i.e. the drugs aren't excreted by the lung unchanged |
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Why are Desflurane, Sevoflurane, and Isoflurane used as anesthetics?
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-They have low B/G ratios, i.e. they are minimally soluble in the blood (Desflurane has lowest B/G)
-Therefore, they kick in more quickly and the patient emerges more quickly -They are not metabolized, i.e. they are mostly excreted by the lung unchanged |
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Why is NO not used as an anesthetic alone?
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The MAC (minimum alveolar concentration) is 105%, requiring the patient to be placed in a hyperbaric chamber and all oxygen to be removed
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What is minimum alveolar concentration (MAC)?
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Alveolar concentration at which 50% of patients do not move purposefully in response to surgical incision
-The MAC is decreased in the elderly, pregnant women, and sick people. |
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Factors that influence induction and emergence of inhaled anesthetics
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1. Lower solubility in blood=faster rise in brain
2. Higher anesthetic concentration=faster rise 3. Need to maintain ventilation, normal is optimal for induction 4. Low cardiac output=faster rise (because less of the drug will be exposed to blood and will dissolve) 5. High concentration in venous blood=faster rise (because can't dissolve anymore drug into the blood) 6. Low blood solubility of drug=faster emergence; conversely if there is a high venous concentration of drug, then will take longer for patient to awaken |
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Pharmacokinetics of intravenous anesthetics
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1. Rapid increase in concentration with bolus=rapid onset
2. Concentration proportional to drug effect 3. Rapid redistribution after bolus=short duration 4. Large doses that fill volume distribution=long duration |
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Physiological Effects of inhaled anesthetics
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1. Cellular metabolism decreases-decreased oxygen consumption, decreased myocardial oxygen consumption, oxygen demand decreases
2. Sympathetic tone decreases-arterial and venodilation, heart contractility decreases, heart rate can be variable depending on reflex 3. Direct sinus node changes, direct aretial dilation, direct decrease in contractility 4. Respiratory: decrease tidal volume, respiratory rate increases, but alveolar ventilation decreases; Response to hypercarbia and hypoxemia decreases; Carbon dioxide apnea threshold increases; potent vasodilators 5. Brain-all functions decrease; increases blood flow (except NO) 6. Renal: GFR decreases with oliguria; ARF unchanged 7. Hepatic flow decreases with decreased cardiac output 8. Muscle tone decreases |
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Toxicity of inhaled anesthetics
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1. Renal toxicity
2. Hepatic toxicity (ex. Fatal Halothane Hepatitis) 3. Respiratory: Sevoflurane can create carbon monoxide via a reaction with the carbon dioxide absorber 4. Malignant hypothermia-The genetic predisposition to a hypermetabolic response to succinylcholine or inhaled anesthetics. Causes rhabdomyolosis, increased T, acidosis, hyperkalemia, and hypercarbia. Use intravenous anasthetics instead. Treat with Dantroline. 5. If have increased intracranial pressure, use intravenous anesthetics and/or NO instead because of the increase in cerebral blood flow |
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Physiological effects of intravenous anesthetics
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1. Cellular metabolism decreases-decreased oxygen consumption, decreased myocardial oxygen consumption, oxygen demand decreases
2. Sympathetic tone decreases-arterial and venodilation, heart contractility decreases, heart rate can be variable depending on reflex 3. Direct sinus node changes, direct aretial dilation, direct decrease in contractility 4. Respiratory: decrease tidal volume, respiratory rate increases, but alveolar ventilation decreases; Response to hypercarbia and hypoxemia decreases; Carbon dioxide apnea threshold increases; potent vasodilators 5. Brain-all functions slowed, but intravenous anesthetics decrease cerebral blood flow (except ketamine) 6. Renal: GFR decreases with oliguria; ARF unchanged 7. Hepatic flow decreases with decreased cardiac output 8. Muscle tone decreases |
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Anesthetic properties of benzodiazapenes/sedatives
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-Cause unconsciousness and amnesia
-Do not produce analgesia -Can reverse with Flumazenil, a partial antagonist, but the respiratory depression is hard to reverse |
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Anesthetic properties of narcotics/opiods
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-Produce analgesiand intense pain relief
-Do not produce surgical anesthesia alone -Their use with an anesthetic can reduce the amount of anesthetic needed -Effects 100% reversible with naloxone, an opioid antagonist |
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Physiological effects of ketamine
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-Produces dissociative anesthesia (will say ouch, but have no emotional or reflex response to pain)
-Patient remains responsive -Stimulates cardiovascular system -Preserves airway reflexes -Short elimination half life -Increases cerebral blood flow -Causes psychosis |
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Propofol:
-Effects -Elimination |
-Is an anesthetic: causes unconsciousness, cardiac and respiratory depression, surgical anesthesia, and death
-Like the other intravenous anesthetics, requires hepatic metabolism; high doses or long infusions fill volume of distribution and require a long time for emergence |
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Tetracaine, Procaine/Novocaine, Chloroprocaine, Cocaine
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Ester class of local anesthetics; sodium channel blockers
-metabolized by plasma esterases, producing para-amino benzoic acid (PABA) -PABA can cause allergic reactions |
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Lidocaine, Mepivicaine, Bupivicaine, Ropivicaine
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Amide class of local anesthetics;sodium channel blockers
-Hepatic metabolism -less incidence of allergic reaction than esters |
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Drugs mixed with local anesthetics
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1. EPI and phenylephrine-vasoconstrictors
2. Preservatives, including methylparaben; metabolites include PABA |
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Increasing nerve susceptibility with increasing concentration of local anesthetics
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1. Pain and Temperature
2. Proprioception, pressure 3. Muscle |
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Toxicity of local anesthetics
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1. Max tolerated dose increased with use of vasoconstrictors, sedative-hypnotic drugs, and with prolongued time of administration
2. Max tolerated dose decreases with hepatic disease 3. CNS toxicity=circumoral tingling, tinnitis, sedation, seizures 4. Cardiovascular toxicity=decreased rate of conduction, contractility, and heart rate |
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Toxicity of neuraxis blocks (epidural, spinal)
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1. Blocking sympathetic nervous system fibers-can lead to hypotention
-If block above T10, very likely to get hypotension because blocking venous return from splanchnic and leg venous beds -If block above T4, can sympathetic fibers to heart from T1-T3, as well as reducing venous return from all major venous beds; cardiac collapse and arrest 2. Contraindicated for patients with decreases coagubility because can cause epidural hematoma 3. Also contraindicated for aortic stenosis and shock patients because of hypotensive risk |
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Dextromethorphan
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-centrally acting antitussive
-very crappy opioid agonist, depresses medullary cough centers -Does not dependence or tolerance, nor does it have analgesic and sedative properties -efficacy questionable |
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Codeine
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-centrally active anti-tussive, depresses medullary cough center; multiple opioid agonist
-Has analgesic and sedative effects; good for relieving a painful cough -Causes drying of mucosal airway secretions, which may be helpful for bronchorrea, but not good if secretions already viscous -causes minimal respiratory depression -Nausea, vomiting, constipation -Can develop addiction and tolerance |
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Non-narcotic centrally acting anti-tussives
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chlophedianol, levopropoxyphene, noscapine
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Narcotic centrally acting anti-tussives
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Hydrocodone, hydromorphone, methadone, morphine
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Demulcents
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-cough drops
-form a protective coating over irritated pharyngeal mucosa; only work above larynx -include acacia, licorice, glycerin, honey, wild cherry syrups |
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Local anesthetics used as anti-tussives
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-Lodicaine, Benzocaine, hexylcaine hydrochloride, tetraciane
-inhibit the cough reflex -used for bronchoscopy or bronchography |
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Benzonatate
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-congener of tetracaine
-local anesthetic used to suppress cough reflex -causes local anesthesia, depression of pulmonary stretch receptors, and non-specific central depression |
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Humidifying aerosols/steam inhalants
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-steam acts as demulcent by coating airway
-Also decreases the viscosity of respiratory secretions by liquifying phlem |
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Iodides (potassium iodide and iodinated glycerol)
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-expectorants that liquefy tenzcious bronchial secretions
-used for late stages f bronchitis, bronchiectasis, and asthma -side effect=acneiform skin eruptions, coryza, erythema of face and chest, painful swelling of salivary glands -long term use can cause hypothyroidism |
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Guaifenesin
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-most commonly used expectorant-breaks up phlem
-efficacy questionable -no adverse effects |
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Ammonium chloride, terpin hydrate, creosote, squill
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-traditional expectorants-break up phlem
-efficacy questionable |
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Acetylcysteine
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-Mucolytic-breaks disulfide bonds in mucus
-Used for liquefying thickm viscous secretions of CF and chronic bronchitis -Given as 10-20% solution as nebulizer or instillation -May cause bronchospasm; given with isoroteronol or other bronchodilator |
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Dornase alfa
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-Recombinant human DNase
-Breaks up DNA, decreasing the viscosity of purulent excretions -This and other proteolytic enzymes can cause irritation of the buccal and pharyngeal oral mucosa and allergic reactions -used for CF |
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Phenylephrine
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-topical (nose spray) decongestant in neosinefrine
-alpha agonist, vasoconstrics nasal blood vessels to open up airways -short acting -can have rebound hyperemia with prolonged use |
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oxametazaline
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-topical (nose spray) decongestant in Afrin
-alpha agonist, vasoconstrics nasal blood vessels to open up airways -short acting -can have rebound hyperemia with prolonged use |
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phenylpropanalamine
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-alpha agonist used as a long acting decognestant and appetite suppressant
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pseudophedrine
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-Long acting alpha agonist decongestant taken orally
-Side effect=increased blood pressure, do not give to hypertension patients -Don't use with MAO inhibitors -Easily converted to methamphetamine; pseudophed over the counter now contains phenylephrine |
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Cromolyn and Nedocromil
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-inhibit mast cell degranulation by inhibitng delayed chloride channels
-use prophylactically for asthma; cannot reverse bronchospasm or bronchial tone -poor GI absorption; delivered topically via inhaled powder or aerosol -also used as nose spray for allergic rhinitis -works better in children, but doesn't work for everyone |
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Theophylline
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-methylxanthine used for asthma
-inhibits phosphodiesterase, which increases cAMP and causes smooth muscle relaxation -Need to monitor plasma concentration to prevent toxicity -side effects=nervousness and tremor; increased heart rate and contractility; increased GI secretion of gastric acid and digestive enzymes; diuretic (like drinking too much coffee) -not first line therapy |
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Names of short acting (3-4 hours) beta2 agonists used for asthma
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Albuterol (Ventolin)
Metoproterenol (Alupent) Terbutaline (Brethine) Pirbuterol (Maxair) |
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Name of long acting (12 hours) beta2 agonist used for asthma
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Salmeterol (Servent)
-can be used prophylactically twice a day |
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Ipratropium bromide
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-Muscarinic antagonist used for COPD
-Given via inhaler; poorly absorbed so no systemic effects -Takes up to 45 minutes for onset, but lasts longer than B2 agonists -Can be given with short acting B2 agonist for immediate relief |
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Predisone and oral corticosteroids for use in asthma
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-Used only in severe, prolonged asthma flareups
-Cannot reverse bronchospasm -Use for only 7-10 days, taper off dosage through out |
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Beclomethasone (Beclovent, Vanceril)
Triamcinolone (Azmacort) Fluticasone (Flovent) |
-inhaled corticosteroids
-used for severe asthma as prophylactic agent -can be used chronically, and can be used with salmeterol -most common side effect=propharyngeal candidiasis (thrush) |
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Zileuton (Zyflo)
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-5-Lipoxygenase inhibitor used for asthma; inhibits production of leukotrienes
-Leukotriene inhibitors only work in 1/3 of patients with asthma |
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Zafirukast (Accolate)
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-Blocks LTD4 receptor
-LT inhibitors only work in 1/3 of patients with asthma |
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Actions of cortisol
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-Break down of protein and loss of muscle mass
-Increase glucose in blood and diabetes -Increased fatty acids in the blood, can cause acidosis -Hypernatremia (and increase in chloride) causing hypertension -Hypokalemia, which can cause arrhythmias and torsades -Anti-inflammatory: Inhibits prostaglandin synthesis, inhibits WBC migration, usually have increase in WBC count because cells can't leave blood and enter tissue -Immunosuppressive, inhibits production of anti-transplant tissue antibodies |
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Adverse effects of cortisol
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-acne (stimulates sebaceous glands)
-Thinning of skin and more visible arteries, veins, and nerves (because destroys CT) -Muscle wasting -Redistribution of fat into back and face -Hyperglycemia -Hypertension -Increased gastric acid secretion, causing a peptic ulcer with our without hemhorrhage -cataracts -psychosis -Bone resorption and osteoporosis, especially in the elderly -Increased susceptibility to infection -Myopathy, though uncommon -Giving large doses over extended period of time can cause iatrogenic Cushing's syndrome |
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Conditions warranting caution when prescribing corticosteroids to patients
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-Peptic ulcer disease
-Osteoporosis -Turberculosis and other chronic infections -psychological disturbances |
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Spironolactone
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-Inhibits aldosterone
-Causes hyponatremia and hypokalemia -Only effective in presence of aldosterone -Used in treatment of primary and secondary aldosteronism |
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Corticotropin
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-ACTH
-polypeptide -made from animal sources, can be antigenic -given IV or IM because not absorbed -t1/2 is 15 minutes, short because of proteolytic blood enzymes -Used in the past for ulcerative colitis, because infused ACTH increases -Now used for diagnoses of adrenal or anterior pituitary or hypothalamic insufficiencies |
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Cushings Disease, Primary Addison's Disease, and Secondary Addison's Disease
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Cushings Disease=Too much cortisol, humpback and moon facies
Primary Addison's Disease: Lack of ACTH released from anterior pituitary, so both cortisol and ACTH low -Secondary Addison's disease: Insufficient adrenal release of cortisol, ACTH is high and cortisol is low |
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Pharmacokinetics of corticosteroids
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-t1/2=6 hours
-Hydroxylated by liver P450 enymes into 17-hydroxysteroids, secreted into kidney -80% bound to transcortin protein or albumin in the blood, 20% free and active -well absorbed, can be supplied orally, injected, or locally |
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Corticosteroid withdrawal
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-Reduce corticosteroid doses gradually
-Can cause adrenal insufficiency -May include fever, myalgia, arthralgia, and malaise |
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Major uses of corticosteroids
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-Asthma: give via inhalation
-Allergic Rxns, like poison sumac (Meldrose Pack) and facial poison ivy -Immunosupression after transplant -Arthritis (1 injection into synovium every 3 months only, because causes bone resorption) -Rheumatoid arthritis -Leukemia -congenital adrenal hyperplasia -other dermatological and opthalmologic diseases -Lupus |
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Hydrocortisone
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-short acting (4-6 hours)
-3x a day -has mineralcorticoid properties (salt retention, hypokalemia) -Least potent anti-inflammatory |
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Prednisone
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-#1 oral steroid because most bioavailable
-very low mineralcorticoid activity -short lasting -giving 20 mg per day replaces all adrenal cortex cortisol production -4 times more potent than hydrocortisone |
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Methylprednisolone
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-used for injection in an nsoluble form that stays in joint; can give injection with lidocaine to prevent irritation
-5x more potent than hydrocortisone -short acting -no mineralcorticoid activity |
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Trimcinolone
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-Insoluble form for injection and topical form
-5x more potent than hydrocortisone -no mineralcorticoid activity -intermediate acting |
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Dexamethasone
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-Long acting (lasts longer than 12 hours)
-no mineralcorticoid acitivity -30 times more potent than hydrocortisone -Injections or inhalers for acute asthma |
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Betamethasone
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-30 times more potent than hydrocortisone
-no mineralcorticosteroid activity -long acting |
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Fludrocortisone
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-10 times more potent than hydrocortisone
-Very high mineralcorticoid activity -Not used |
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First line drugs used for TB
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-Rifampin
-Isoniazid -Ethambutol -Pyrazinamide |
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Second line drugs used for TB
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-Streptomycin (aminoglycoside)
-Floroquinolones: Moxifloxacin, gatifloxacin -Amikacin, Kanamycin (aminoglycosides) -Capreomycin -Cycloserine -Ethionamide -P-aminosalicylic acid |
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Rifamycins
-Names of Rifamycin drugs -Mechanism of action |
-Rifampin, Rifabutin, Rifaximin
-Inhibit RNA polymerase, preventing transcription |
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Rifamycins ADME
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-High availability, except Rifaximin (not absorbable)
-Highly distributed, including to CNS fluids -Causes secretions (tears, sweat) to be colored orange-red -Metabolized in liver by de-acetylation -VERY strong cytP450 inducer -Largely excretred by biliary tract; goes through enterohepatic recirculation and 30% excreted renally |
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Rifamycins
-Effective against which bacteria? -Resistance profile |
-Very effective against M. tuberculosis
-Also effective against staph and eneteric Gram negative rods -Spontaneous resistance is common; do not use as a monotherapy |
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Adverse effects of Rifamycins
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-P450 induction (Rifampin induces more than Rifabutin); includes induction of CYP 3A4
-N/V -Rash -Hypersensitivity, notably fever -Hepatotoxicity |
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Uses and Indications of Rifamycins
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-Rifampin is a cornerstone of therapy inTB
-Rifabutin is an alternative to Rifampin; also used for M. avium-intracellurae complex (MAC) infections -Never use Rifampin and Rifabutin as monotherapy for TB -Rifaximin not absorbable and not used for TB; used for local GI tract infections |
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Isoniazid (INH)
-Mechanism of action |
-Specific to mycobacteria: Inhibits synthesis of mycolic acids needed for their cell wall
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Isoniazid ADME
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-Highly absorbed
-Well distributed, including to CNS secretions and TB lung consolidations -Variable metabolism via acetylation by NAT2; Japanese and Inuit population are rapid acetylators and Jews and Scandinavians are slow acetylators -Metabolites excreted renally |
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Uses for Isoniazid
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-Active only against M. tuberculosis and M. kansasii
-Bacteriostatic against non-dividing organisms and bacteriacidal against dividing organisms -Drug of choice for both latent and active TB |
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Isoniazid drug interactions
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-Minimal (unlike Rifampin)
-Interaction with phenytoin, need to monitor phenytoin concetrations, not cytP40 related |
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Adverse effects of isonazid
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-Rash, fever
-Drug-induced lupus (goes away when stop drug) -Hepaotoxicity -Neurotoxicity: -Peripheral neuropathy, prevent or treat with pyridoxme (B6) -Optic neuritis, seizures |
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Ethambutol (EMB)
-Mechanism of action |
Inhibits arabinosyl transferase, prevents arabinogalactan synthesis needed for cell wall
-Only active against mycobacterium |
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Ethambutol ADME
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-Highly absorbed
-Widely distributed, including in CSF secretions -Some metabolism, not cytP450 -Renally eliminated |
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Ethambutol uses
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-First line drug used for TB and MAC infections
-Do not use as monotherapy; resistance not common, but will develop if use by itself |
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Ethambutol drug interactions
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-Minimal
-Optic neuritis: Decreased vision with loss of red-green differentiation; need to test visual acuity during long term therapy -GI effects -Rare CNS effects |
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Pyrazinamide (PZA) mechanism of action
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-Inhibits FAS2, bloccking synthesis of fatty acid precursors needed for cell wall
-Active only at acidic pH -May be bactericidal or bacteriostatic |
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Pyrazinamide ADME
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-Highly absorbed
-Widely distributed, including in CSF fluids -Metabolized hepatically, but not by CYP450 -Renally eliminated mostly as metabolites |
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Uses of pyrazinamide
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-Only active against TB
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Adverse effects of pyrazimamide
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-Hepatotoxicity
-Hyperuricemia and gout -Arthalgias -GI effects |
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Streptomycin
-Mechanism of acton |
-Aminoglycoside antibiotic
-Inhibits protein synthesis by binding to 30S ribosomal subunit; causes misreading of mRNA -Bacteriostatic for TB, although bacteriocidal for most organisms |
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Streptomycin ADME
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-Poorly absorbed; must be given IV or IM
-Moderate distribution; Poor distribution in CNS fluids; moderate distribution to lungs -No metabolism -Entirely renally eliminated and very nephrotoxic |
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Uses of Streptomycin
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-Active against TB, but not intracellular TB
-Used as second line therapy for TB -Active against many other Gram negative rods and Gram positive cocci |
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Adverse reactions of streptomycin
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-Nephrotoxicity: need to monitor urine output, serum creatinine, and streptomycin concentrations
-Ototoxicity: both auditory and vestibular; not reversible |
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Kanamycin and Amikicin
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-Aminoglycoside antibiotics
-Resistance to these drugs not linked to streptomycin resistance |
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Cycloserine
-Mechanism of action -Uses -Adverse effects |
-Inhibits ala-ala synthetase and alanine racemase, preventing peptidoglycan monomer synthesis at 2 different steps
-used as second line agent for TB; resistance is common -Adverse effects: Psychosis and peripheral neuropathy that is somewhat preventable by Pyrodixime (B6) adminstration |
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Floroquinolones used against mycobacterium
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-Moxifloxacin and Gatifloxacin; Levofloxacin also used
-Moxifloxacin causes less hepatotoxicity -Also active against MAC infections -Currently second line therapy, but may move up |
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p-Aminosalicyclic acid
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-Second line therapy for TB
-Resembles PABA, blocks folate synthesis -Relatively safe, but high incidence of hypersensitivity |
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Ethionamide
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-Smilar to isoniazid, but less effective and used as second line therapy against TB
-Resistance to isoniazid causes resistance to ethionamide |
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Capreomycin
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-Second line therapy for TB
-causes oto toxicity and nephrotoxicity |
