Pharm Unit 2 - Shelbye's CSON Notes Blog
Pharm Unit 2
Special concepts r/t Antimicrobials
• Selective toxicity
– Ability to target without harming host
• Susceptibility
• Prophylaxis
– Neutropenia, Surgery, Endocarditis
• Combination Therapy
• Misuse – non-specific fevers, viruses
Resistance
Ch. 86
Aminoglycosides: Background
• Resistance is beginning to limit use
– Gentamicin – cheaper but commonly used
– 20 diff aminoglycoside-inactivating enzymes
– Reserve amikacin
• Bactericidal
– concentration dependent
– Post-antibiotic effect – several hours (prolonged)
– NOT effective against anaerobes
|Gentamicin (Garamycin) |
|MOA/ Use |Narrow spectrum for gram negative bacilli- especially pseudo. Aerugenosa, E. coli, Klebs, Serratia |
|ADME |Poor CSF |
| |Not absorbed orally |
| |Toxicity with wound irrigation |
| |Binds tightly to renal tissue |
| |Excretion primarily renal |
| |Dosage varies widely (.5 mg/kg to 25 mg/kg) |
|Adverse Effects |Ototoxic |
| |R/t excess trough levels- sensory hairs |
| |HA, N, vertigo then high- pitched tinnitus (action?) |
| |Vestibules of ears and absorbs into tissues to kidney |
| |Nephrotoxic |
| |Total cumulative dose |
| |ATN (acute tubular necrosis- leads to renal failure) -- proteinuria, casts (slough or big particles), increased BUN,|
| |increased Creatinine |
| |Elderly and children at risk |
| |Neuromuscular blockade |
| |Flaccid, weak muscles |
| |Dosage based |
| |Neurotoxic with peripheral muscles |
| |Hypersenditivity & blood dyscrasias (rare) |
|D = D |PCNs, Cephs, Vanco used in combo |
| |PCNs inactivate – schedule issue? |
| |Ethacrynic Acid – ototoxicity |
| |Other nephrotoxics |
| |Skeletal Muscle relaxants |
Aminoglycosides: Special concerns
• Neomycin most nephrotoxic
• Scheduling once daily – Safer?
– Post-antibiotic effect
– Washout – esp. in vestibule and kidneys
– Typically only measure trough – up to 1hr prior to next dose – level should be ?
Ch. 91 Antifungal Agents
Systemic mycotic infections
• Opportunistic (host is immunocompromised, malnourished, ill): candidiasis, aspergillosis, cryptococcosis, mucormycosis
• Nonopportunistic: sporotrichosis, blastomycosis, histoplasmosis, coccidioidomycosis
Superficial mycotic infections
• Candidiasis
• Dermatophytes
Major Classes of Antifungals
• Polyenes
• Azoles
• Pyrimidine analogs
• Echinocandins
|Amphotericin B (Fungizone) |
|MOA/ TE |Broad spectrum antifungal agent binds to ergosterol component of fungal cell wall and increases permeability. |
| |DOC for most progressive, potentially fatal systemic mycoses |
|ADME |Highly toxic (sterols) |
| |Poor GI absorption - SLOW IV USE ONLY |
| |Poor CSF |
| |Break down human sterols and bug sterols |
|Adverse effects – almost 100% - varying |Phlebitis |
| |Fever, chills, nausea – pre-treat w benadryl / acetaminophen |
| |Nephrotoxicity – residual if (4 g/day, 1 L NS, Monitor q 3-4 days |
| |Hypokalemia |
| |Bone marrow suppression |
|D(D |nephrotoxics - flucytosine |
|Itraconazole (Sporanox) |
|MOA/ TE |Azole group of antifungal agents that inhibits sythesis of ergosterol – fungistatic to treat histoplamosis, meningitis |
| |of cryptococcus neoformans & disseminated candidiasis |
|ADME |PO or IV |
| |Food ( abs. capsules, ( abs. of suspension |
| |Metabolized in liver |
| |40% excreted unchanged in urine |
|Adverse Effects |Common – N, V, and D, rash, HA, edema |
| |Rare - Hepatic necrosis, transient cardiosuppression |
|D(D |Inhibits cytochrome P450 isozymes |
| |Increases levels of warfarin, digoxin, sulfonylureas, cyclosporine, quinidine and many other drugs |
| |Acid reduces decrease drug levels |
| | |
| |**if system is impaired, drug levels will rise (cytochrome P450 isozymes) |
Azoles: Special Considerations
• Fluconazole [Diflucan]
– Lower toxicity level
– Can be taken orally
– SJS syndrome (Stephen Johnson syndrome)
• Ketoconazole [Nizoral]
– Effect on sex hormones – inhibits production
Drugs for Superficial Mycoses
• Dermatophytic infections (e.g., ringworm)
– Tinea pedis, tinea corporis, t. cruris, & t. capitis
• Drugs
– Clotrimazole (Gyne-Lotrimin) – DOC for topical dermatophytic and candida infections of skin, mouth, vagina
• Vulvovaginal candidiasis
– Griseofulvin (Grifulvin) - oral
• onychomycosis
|Griseofulvin (Grifulvin V) |
|MOA/ TE |Superficial mycoses only – inhibits fungal mitosis – incorporates into keratin |
|Adverse Effects |Transient headache, rash, GI |
| |Contraindicated in hepatocellular disease |
|D(D |Decreases warfarin |
Ch. 92 Drugs fro Non-HIV Viral Infections
Viral Infections
• Dilemma
• Types
– HSV (Herpes-simplex)
• Genitalia, mouth, face (HSV-2)
• More sensitive to antivirals, less resistant
– VZV (Varicella Zoster)
• Chicken pox – Shingles
• Moderate sensitive
– CMV (Cytomegalovirus)
• Less sensitive and more resistant
|Acyclovir (Zovirax) |
|MOA/ TE |Suppress synthesis of viral DNA and is useful in treating HSV1,2 & VZV – no cure |
|Adverse Effects |Intravenous: reversible nephrotoxicity, phlebitis |
| |Infuse slowly – hydration – during & 2 hr after |
| |Oral: GI, vertigo |
| |Topical: stinging |
|Nursing Implications |Resistance – type of clients |
| |IV indicated for oral lesions in |
| |STI control |
| |Treatment for VZV in elderly and children (w/in 24 hr) |
| |ONLY give po (low availability), topically or IV |
| |NO IV bolus, NO IM, or NO SubQ injections |
| |Valacyclovir [Valtrex] – prodrug that increases oral bioavailability by 55% |
| |Without regard to meals |
| |*check to see if admin is correct in book |
| |Bolus- def. |
|Ganciclovir (Cytovene, Vitrasert) |
|MOA/ TE |Suppresses replication of viral DNA to treat CMV retinitis of immune compromised clients & prevent CMV in transplant |
| |patients |
|Adverse Effects |Granulocytopenia & thrombocytopenia |
| |Mutagenesis, carcinogenesis |
| |Teratogenisis and infertility – (90d following cessation) |
| | |
|Valganciclovir (Valcyte) – prodrug for oral |Take intact – with food |
|use | |
Hepatitis C (HCV)
• Transmission—blood and semen
• Typically asymptomatic
• Leading cause for liver transplants
• Among most common causes of liver cancer
• Not curable, only suppressible
• Drugs
– Pegylated interferon alfa combined with ribavirin
|Interferon alfa (Peg-Intron) |
|Immune modulatory, antineoplastic, antiviral |
|MOA/ TE |Blocks entry of virus, synthesis of viral m-RNA and proteins, and viral assembly. Tx of chronic Hep B & C |
|ADME |Pegylated - makes drug longer acting |
| |Only parenterally (SubQ) |
|Adverse Effects |Flu-like (fever, myalgia, HA, fatigue) & depression |
| |Long/High dose – thyroid dysfunction, heart damage, bone marrow suppression |
| |Alopecia, GI, injection site pain, bruising |
|Ribavirin (Rebetol) |
|MOA unclear |Used with Interferon A - together are DOC for Hep C (HCV). |
| |Therapy 24 to 48 weeks. Goal is SVR – sustained virologic response (loss of detectable viral |
| |RNA) |
|Adverse Effects |Hemolytic anemia (a lot of RBCs that are broken) |
| |Teratogenic (Category X) – two forms of BC |
|Dosage |Based on weight |
|Teratogenic |Can kill fetus |
Hepatitis B - HBV
• Transmission—blood and semen
• Drugs
– HBV vaccine
– Interferon alfa-2b [PEG-Intron]
– Lamivudine [Epivir-HBV]- already developing resistance
– Adefovir [Hepsera]
• Duration of treatment and relapse
Flu Vaccines
• 3 strains – selected by CDC, FDA, & WHO
• Inactivated
– IM
• Live attenuated – LAIV (Flumist) – 2003
– Intranasally
– MUST BE FROZEN
– Only ages 5-49
• Efficacy – Who should receive it?
– 1-2 wks before exposure & lasts for 6 mo
• Adverse effects
– Fever, malaise, myalgia
– Guillain-Barré syndrome – Swine flu vac. 1976
– LAIV – runny nose, HA, cough – rare GBS, anaphylaxis
• Precautions and contraindications
– Acute febrile illness, hypersensitivity to eggs
• Who should NOT without MD approval?
– Allergy to egg
– Previous severe reaction
– GBS
– Moderate, severe illness w/ fever
– Children under 6 months
– LAIV not for: adults over 50, children under 5, pregnants, children or adolescents on long-term ASA therapy, chronic heart, lung disease
Drugs for Influenza
|Oseltamivir (Tamiflu) |
|MOA/ TE |inhibit viral replication of Inf A&B and is used to prevent and treat same – effective if implemented within 2 |
| |days of sxms |
|Adverse Effects |N&V |
| |Confusion, self injury |
|Expensive |Must be started prior to 48 hr |
ATI p. 220 Ch. 32 Antidepressants
General Points
• Most common psychiatric disorder
• Major treatment method - medications
– Five major groups
• Goal?
• Sxms
– Depressed mood, loss of pleasure / interest in all or nearly all of one’s usual activities
• Under-treated
• More prevalent in women
• Suicidal thoughts may increase w Rx
Tricyclic Antidepressants (TCAs)
|Imipramine (Tofranil) |
|MOA/ TE/ Use |Blocks reuptake of the MAO transmitters NE (norepinephrine) and serotonin. Elevates mood, thereby treating |
| |depression. |
| |Other uses: bipolar disorder, neuropathic pain, insomnia, fibromyalgia, OCD |
|Adverse Effects |Orthostatic hypotension, sedation, anticholinergic effects, diaphoresis, cardiotoxicity, seizures, hypomania, |
| |“yawngasm”- orgasm that occurs when they yawn |
|Glands (Table 14-1) |Salivary glands- decreased secretion |
| |Sweat glands- decreased secretion |
| |Bronchial glands- |
|Precautions/ Interactions |TCAs w MAOI can lead to severe HTN |
| |Potentiates drugs like NE (norepinephrine) |
| |Potentiate CNS depressants |
|Antidote |Activated charcoal after gavage |
|Dosing |Based on clinical response – don’t give more than a week supplys |
| |Dose at bedtime once levels achieved – EXCEPT in elderly (cardiac reasons) |
SSRI Antidepressants
|Fluoxetine (Prozac) |
|MOA/ TE/ Use |Selective serotonin re-uptake inhibitor resulting in elevated serotonin levels – elevating mood and relieving |
| |depression. |
| |Helps in bulimia nervosa |
|Adverse Effects |Impotence, weight gain, Serotonin syndrome, withdrawal syndrome, EPS, bruxism (clenching teeth and jaw), bleeding, |
| |hyponatremia. |
| |Some people have w/draw symptoms with this |
|Interactions |MAOIs, Warfarin, & TCAs |
MAOI Antidepressants
|Phenelzine (Nardil) |
|MOA/ TE/ Use |Enzyme – deactivates NE, serotonin, dopamine, and tyramine (NE stimulator) from foods |
| |NOT 1st CHOICE |
| |Relevant P-kinetics |
| |Tyramine |
|Adverse Effects |CNS stimulation – agitation – hypomania – mania – hypotension – HTN crisis – meperidine (hyperpyrexia) |
| | |
| |Deactivates tyramine which deactivates the transmitter |
Atypical Antidepressants
|Bupropion (Wellbutrin) |
|MOA |Action unclear |
|Effect |Stimulant ergo no wt gain |
| |No sexual dysfunction – may augment |
|Adverse Effects |agitation, HA, dry mouth, constipation, wt loss, insomnia, tachycardia, seizure |
|Note |St. John’s Wort (Box 32-2) |
|Other |Used in smoking cessation |
| |Known to bring on seizures |
| |Can enhance sexual functions |
| |Consider this a vitamin (herbal supplement) |
|(ATI p. 203 or 220??) |May have an impact with BCP |
Ch. 34 Classification: Sedative- Hypnotics
Overview
• Venacular
– Anti-anxiety, anti-anxiolytics, tranquilizers
– Hypnotics
• Major Categories
– Benzodiazepines, Barbiturates, Barbiturate–Like
– Miscellaneous
• Major Effects
– CNS depression
• Therapeutic Uses
– Relieve anxiety, facilitate sleep, manage muscle spasms, seizure and panic disorders, augment anesthesia, and manage ETOH withdrawal
Benzodiazepines (CIV) Category D
|Diazepan (Valium) – self limiting |
|Others: clonazepam, lorazepam, clorazepate |
|MOA |Depress neuronal function at multiple CNS sites by potentiating endogenous GABA (gamma-aminobutyric acid) and is |
| |limited because GABA is finite(safer |
|Cardiac |PO effect - heart & blood vessels (not a huge effect) |
| |IV effect – potentially ? (huge effect) |
|Respiratory |Minimal alone, serious if combo or IV |
|Pharmacokinetics |Readily absorbed |
| |Differ in respect to time - course of action |
| |(main indicator for which one chosen for which job) |
|Adverse Effects |CNS – daytime vs. nighttime impacts |
| |Amnesia |
| |Paradoxical- opposite effect |
| |Abuse |
| |Malnutrition, liver disease and blood levels |
|D(D |w/ other CNS depressants |
|Dosage |varies by agent |
|Low Albumin |Low circulation of drug (malnutrition) |
Nursing Implications ATI p. 218
Benzodiazapine-likes
|Zolpidem (Ambien) CIV |
|MOA/ TE/ Use |Agonists at benzodiazepine receptor site on GABA channel prolonging sleep |
| |duration and helps relieve insomnia |
| |Low potential for tolerance or abuse |
|Adverse Effects |Causes sleep walking, or not safe effects for the person |
| |Similar to benzodiazepines (daytime drowsiness / dizziness) |
| |Can intensify CNS depressants |
|Dosage/ Administration |Before bedtime?- about 1 hr before bedtime |
Melatonin Agonist
|Ramelteon (Rozerem) |
|MOA/ TE/ Use |Activates melatonin receptors and rapidly induces sleep to treat insomnia |
|Adverse Effects |Somnolence, dizziness, and fatigue, reduced libido |
|Precautions |ETOH, liver impairment, dangerous activities |
Barbiturates
|Secobarbital (Seconal) |
|MOA/ TE/ Use |Mimics GABA and depresses CNS directly causing relaxation and anxiety reduction. |
| |Other uses: seizure management, anesthesia, sleep disorders, mania |
|ADME |NO CEILING TO LIMITS OF CNS depression (mimics GABA) |
|Adverse Effects |Resp. depression, hypotension in toxic doses, can readily cause death |
|Precautions |Highly addictive - physical dependence – withdrawal can be severe |
| |Caution in elderly |
| |Caution with other CNS agents |
| |Caution with IM injection |
Ch. 37 Drug Abuse
Terms
• Drug abuse- using a drug in a fashion inconsistent with medical or social norms
• Addiction- a disease process characterized by the continued use of a specific psychoactive substance despite physical, psychologic, or social harm
• Cross-tolerance- is a state in which tolerance to one drug confers tolerance to another
• Psychological dependence- an intense subjective need for a particular psychoactive drug
• Physical dependence- a state in which an abstinence syndrome will occur if drug use is discontinued
• Cross-dependence- refers to the ability of one drug to support physical dependence on another drug
• Withdrawal syndrome- a constellation of signs and symptoms that occurs in physically dependent individuals when they discontinue drug use
Table 37-1 Diagnostic Criteria for Substance Abuse and Dependence
Ch. 28 Classifications: Opioid (Narcotic) Analgesics, Opioid Antagonists, Non-opioid Centrally Acting Analgesics
Intro to Opioids
• Chemical class: Opioid vs. opiate
• Functional class: Narcotic Analgesic
• MOA – body peptides (3) enkephalins, endorphins, dynorphins
• Opioid receptors - mu, kappa, and delta
– Agonist, partial agonist, antagonist
• Partial agonist- partially mimics, if give with drug can compete with another drug and negate it or antagonize it--- produces low to moderate activation alone
– Strong and moderate to strong
Table 28-1 Important Responses to Activation of Mu and Kappa Receptors
Opioid Agonists
|STRONG: Morphine (Duramorph) CII |
|MODERATE to STRONG: Codeine (Paveral) CIII |
|MOA/ TE |Mimics action of endogenous opioid receptors (mu) to produce analgesia and thereby relieve pain |
| |Other effects include drowsiness, mental clouding, anxiety reduction, sense of well-being |
|Adverse Effects |Resp. depression |
| |Diminished by “tolerance” |
| |Most common cause of OD death |
| |Others |
| |Constipation, orthostatic hypotension, urinary retention / urgency, cough suppression, biliary colic, emesis (usually |
| |with codeine), elevated ICP (intracranial pressure), dysphoria, sedation, miosis, neurotixicity, immune and hormone |
| |suppression with prolonged use |
| |Toxicity |
| |Classic triad (coma, resp. depression, pinpoint pupils) |
|DON’T USE |Caution: don’t use morphine with head injuries – if there is pressure in the head, the vessels constrict |
|ADME (pharmacokinetics) Nursing Implications|Given by several routes |
| |Slowest to fastest |
| |Time-frame for TE varies by mode of administration |
| |Denatured in liver |
| |Hard to cross blood-brain barrier |
|Precautions/ Contraindictions |Decreased resp reserve, pregnancy, head injury, infants / elderly, hypotension, liver disease |
|Interactions |CNS depressants, antihistamines, antihypertensives, MOAIs*, antiemetics, amphetamines, agonist-antagonist, antagonists |
|Dosage |Highly individualized (Table 28-5) |
|Administration |po, IM, IV, SQ, topical |
| |Oral associated with chronic |
| |Preferably fixed schedule |
| |Site specific – hazards- epidural- effects delayed |
Miosis- pinpoint eyes (constriction)[pic]
Mydriasis- linked to dialated eyes[pic]
Other strong opioids
|Fentanyl (Sublimaze) |Anesthesia primary use (injectable) |
| |100 X mg potency of morphine |
| |Commonly seen as transdermal |
| |No children under 2 / none for under 18 less than 100 lbs. |
|Transmucosal (popsicle) |Breakthrough cancer pain |
| |Store carefully |
| |very large amts of drug |
|Meperidine (Demerol) |Interacts with several drugs |
| |Toxic metabolite |
| |Avoid use past 48 hrs and not to exceed 600mg/24hr. |
|Hydromorphone (Dilaudid) | |
|Methadone | |
|Heroin |Crosses blood-brain easier |
Moderate to Strong Opioid Agonists
|Codeine |Usual dose of 30 mg = about same relief as 325 mg of ASA or Tylenol |
| |Combo meds more effective |
| |Extremely effective cough suppressant at 10 mg dose range |
|Oxycodone (OxyContin) & CR forms | |
|Hydrocodone (Lortab, Norco) CIII | |
|Proproxyphene (Darvon, Darvocet) CIV | |
Special Clinical Concepts r/t Use of Opioids
• Pain assessment – including evaluation!
• Dosing amt and schedule
• Fear of addiction in clinical setting
• Avoiding withdrawal – 20 days or more
• Patient controlled anesthesia (PCA)
• Morphine: DOC - heart attack (MI)
• Meperidine [Demerol]: DOC OB in delivery
• Avoid opioids in Head Injury…
Nursing Implications (ATI p. 133 or 150)
Class: Opioid Agonist- Antagonists (Partial agonist)
|Pentazocine (Talwin) |
|Others: nalbuphine (Nubain), butorphanol (Stadol) |
|MOA |act mostly at mu, kappa receptor to produce analgesia and relieve pain |
| |Alone = agonist action |
| |With agonist = can antagonize (blocks mu receptor) |
|Adverse effects |Similar to opioids |
|ADME (Pharmacokinetics) |Less respiratory depression, low abuse potential |
| |Less effective pain relief |
| |*Can start withdrawal sxms in opioid addiction |
Class: Opioid Antagonists
|Naloxone (Narcan) |
|MOA/ TE/ Use |competes for opiate site and blocks effects of opioid agonists / agonist-antagonists – no significant effect given |
| |alone – resulting in REVERSAL of narcotic |
|ADME |Rebound effect – if you give morphine and narcan- the narcan may wear off first |
|Adverse effects |Acute withdrawal |
|Dosage/ Admin |0.4 mg IM, IV, SubQ |
|Others |Naltrexone (ReVia) ETOH/ Opioid abuse |
Non-Opioid: Centrally Acting Analgesics
|Tramadol (Ultram) |
|Others: clonidine (Duraclon) – pain/ HTN |
|MOA/ TE/ Use |Analog of codeine – binds w mu receptor producing analgesia to relieve pain- also blocks re-uptake of norepi (fight or |
| |flight or increase BP) |
|ADME (Pharmacokinetics) |Minimal potential for dependence or resp depression |
|Adverse effects |Rare – most common: sedation, dizziness, HA, dry mouth, constipation |
|Precautions |Can intensify other CNS dep. – ABSOLUTELY avoid MAOIs |
Ch. 77 Laxatives
Bulk-forming
|Methylcellulose, phyllium (Metamucil) |
|MOA/ Use |Behave like dietary fiber – nonabsorbable – swell to form viscous solution / gel and softening fecal mass and |
| |increasing transit. |
| |Temp relief of constipation, diarrhea, irritable bowel, ostomies |
|Adverse effects |Esophageal & intestinal obstruction if not enough fluid ( ? |
| |(If this, then?) |
| |Can obstruct (build a brick) the gut and won’t move through, therefore causing surgery |
| |Esophagus- if you don’t drink enough to get pill down it can cling to walls and get stuck causing tears |
Surfactants
|Docusate sodium (Colace) |
|MOA/ Use |Lower surface tension of stool and softens by facilitating penetration of water into the feces |
| |Act on intestinal wall to inhibit fluid absorption and stimulate secretion of water and electrolytes into the |
| |intestinal lumen. |
|ADME |Full glass of water |
| |Sit upright for 30 min |
| |Effectiveness dose related (min 200 mg/day) |
|Dosage |50-500 mg daily |
|Adverse reactions |Rare |
|Other |Bring water to the stool to soften it |
| |Typically see someone getting 200+ mg/day |
| |New EBP says that anything under 200 is not effective |
Stimulants
|Bisacodyl (Dulcolax), Senna (Senekot) |
|MOA/ Legitimate Uses |Directly stimulate gut motility, increase secretion of water and ions into intestine, and reduce water and electrolyte |
| |absorption. |
| |Uses: Treatment of (1) opioid-induced constipation and (2) slow transit constipation |
|Dosage |related to formulation administered |
| |Take bisacodyl no sooner than 1 hour after ingesting milk or antacids – do not crush |
|Adverse reactions |bowel rupture can occur |
Osmotics (Salt prototypes)
|Sodium phosphate (Fleet) & Magnesium salts |
|MOA/ Uses |Non-absorbable and retains water in the colon |
|Adverse reaction |Dehydration, diarrhea and loss of water (more with salts than with glycol) |
| |Magnesium can accumulate to toxic levels in renal failure |
| |Sodium can retain fluid – so…. Contraindicated in patients with heart failure HTN and edema |
|Other |glycol (MiraLax) – fewer side effects / safer |
Miscellaneous
• Lactulose- sugar base
– Action / Uses
• Poorly absorbed and cannot be digested – by product of breakdown results in osmotic diuresis
• Enhances excretion of ammonia in liver failure
– SEs – flatulence, cramping
• Glycerin Suppository
• Polyethylene Glycol-Electrolyte (GoLytely)
– Safe in dehydrated or electrolyte sensitive
Additional Nursing Implications
• High risk patients
– Contraindicated in abdominal pain, nausea, cramps, regional enteritis, diverticulitis, ulcerative colitis, acute surgical abdomen, fecal impaction, bowel obstruction.
• Abuse
• Castor oil (powerful stimulant – avoid at night – not to children) p. 908
Ch. 69 Antihistamines
Background
• Histamines – (Predominantly H1)
– Endogenous
– Vessel effects
– Bronchi effects
– Stomach effects
– Greatest interest
• Allergic reactions (mild / anaphylaxis)
• PUD
Histamine Release
• Allergic response
– Requires IgE antibodies
– Prior exposure to allergen
• Non-allergic – direct stimulation of cells
– Some drugs, chemicals, radiocontrast media, plasma expanders - require no prior exposure
– Cell injury
Physio/ Pharm Effects
• H1 Stimulation
– Vasodilation (If this, then?)
– Vessel wall cells contract (If this, then?)
– Bronchoconstriction (If this, then?)
– Itching & pain
– Mucus secretion
– CNS effect – cognition / memory / sleep
• H2 Stimulation
– Secretion of gastric acid (If this, then?)
• H2 blocker, block secretion of acid
Allergies & Pharmacology
• Mild Allergy
– Hay fever, urticaria, mild transfusion rx.
– Sxms caused by ? TX?
• Severe
– Anaphylactic shock (bronchocontriction, hypotension, & edema of glottis)
– Sxms caused by? TX? (ch 17)
• Other Uses
– Common cold – runny nose
|Antihistamines: 1st Generation |
|H1 Antagonists (classic antihistamines) |No single prototype |
| |dyphenhydramine [Benadryl] |
| |Highly sedating |
|MOA |Blockers (1st Gen) |
| |Selectively bind to histaminic receptors |
| |Can also bind to nonhistaminic receptor (muscarinic) |
|TE |Vessels (If blocks histamine, then ?) |
| |Capillaries (If blocks, then ?) |
| |Sensory nerves (If, then) – itching relief |
| |Mucous membranes (If, then) |
| |If you block mucous production, then you get dryness |
| |CNS |
| |Therapeutic doses (If, then) - sedation |
| |Overdose – stimulation, seizures – esp. in young |
| |Other: relieve N & V, motion sickness |
|Clinical uses |Mild allergies, seasonal rhinitis, acute urticaria, allergic conjunctivitis, mild transfusion reactions |
| |Some block muscarinic & H1 receptor sites – useful for motion sickness |
| |promethazine [Phenergan] and dimenhydrinate [Dramamine] |
| |Insomnia (diphenhydramine [Benadryl]) |
|Adverse effects |CNS |
| |Sedation = to excess ETOH (If this, then?) |
| |Dizziness, lack of coordination, confusion |
| |Paradoxical: insomnia, excitation, tremors, convulsions |
| |GI |
| |N, V, Diarrhea / constipation, loss of appetite |
| |Anticholinergic effects (memorize) |
| |Cardiac Dysrhythmias w some 2nd Gen. |
| |Torsades de pointes, V-fib |
| |terfenadine [Seldane] & astemizole [Hismanal] (neither one is on market anymore) |
| |Contraindications – third trimester |
| |Precautions: asthma (bronchoconstriction- spasms), children/elderly, urinary retention, HTN, OA glaucoma, prostatic |
| |hypertrophy |
| |Dry mouth, throat, nasal passages, thickened secretions, (cautions?), urinary histiancy, constipation, palpitations |
|D ( D |ETOH, barbs/benzos/ opioids |
|Toxiciy |Sxms similar to atropine poisoning (anticholinergic), hyperpyrexia (fever) |
| |Can lead to death in children via excitation, hallucinations, convulsion, coma, CV collapse, death. |
| |Tx: remove and support – may use charcoal followed with cathartics |
|Antihistamines: 2nd Generation |
|Prototypes |Fexofenadine (Allegra) – Expensive |
|MOA/ TE |Antagonists of histamine to relieve sxms of allergic rhinitis and urticarias |
|ADME |Do not readily cross B-B barrier therefore non-sedating w minimized anticholinergic SEs |
|Precautions |ETOH, drowsiness, liver, kidneys |
Ch. 75 Drugs for Treating Allergic Rhinitis, Coughs, Colds
|Allergic Rhinitis |
|Review of Sxms |Sneezing, itching, runny nose, congestion |
| |Common- conjunctivitis, sinusitis, asthma |
|Commonly associated disorders | |
|Seasonal vs. Perennial | |
| | |
|Outdoor vs. indoor | |
Antihistamines
• First line - oral
• Prophylaxis first
• No use against cold
• Adverse effects
– 1st gen - sedation, anticholinergic
– 2nd gen - rare
Intranasal Glucocorticoids
|Fluticasone (Flonase) |
|MOA/ Use |Predominantly local anti-inflammatory |
| |First line - Most effective against all sxms |
|Adverse effects |Drying, burning, or itching |
| |Rare - sore throat, epistaxis and HA |
| |Rare - systemic – adrenal suppression / slowed growth in children |
|Dose |Adults – 2 sprays of 50 mcg. once daily |
Intranasal Cromolyn
|Cromolyn (NasalCrom) |
|MOA/ Use |Suppresses release of histamine |
| |Best suited for prophylaxis |
| |May not see results for week or more |
|Adverse effects |Negligible |
Sympathomimetics (Decongestants)
|Phenylephrine (Neo-Synephrine) |
|MOA/ Use |Topical - rapid and intense |
| |Oral - prolonged, moderate, systemic effects |
| |Also used in sinusitis and colds |
|Adverse effects |Rebound congestion |
| |CNS stimulation |
| |Cardiovascular |
| |Hemorrhagic stroke w/ phenylporpanolamine (not on market anymore) |
| |Abuse (pseudoephedrine and ephedrine) |
| |Cocaine |
| |Mimics the synthesetics |
|Nasal sprays |2 – 3 sprays every 4 hours needed – not to exceed 5 consecutive days |
| |Use temporarily |
| |Don’t want tissues to become dependant on it |
| |Don’t want them to think they have to have it for tissues to function |
Anticholinergics
|Ipratropium bromide (Atrovent) |
|MOA/ Use |Blocks cholinergic receptors and inhibits secretions to relieve rhinorrea in allergic rhinitis and asthma |
| |No systemic effects |
|SEs |Drying, irritation |
Leukotriene Antagonist
|Montelukast (Singulair) | |
|MOA/ Use |Blocks binding of leukotrienes to receptors thereby relieving nasal congestion |
|Adverse effects |None significant |
Treatment of Coughs
Antitussives
• Antitussives (cough suppressants)
– Actions / use: elevate cough threshold in common cold and URTI
• Opioid (codeine and hydrocodone) - best
– Dosage: codeine 10 to 20 mg up to 6 times daily
• Nonopioid (dextromethorphan) - best
– Opioid derivative w/o euphoria or dependence
– Can lead to mind-body dissociation equal to PCP
Expectorants
|Guaifenesin (Mucinex) |
|MOA/ Use |Increases flow of respiratory tract secretions |
Mucolytics
|Acetlcysteine (Mucomyst) |
|MOA/ Use |Directly thins secretions |
|ADME |Inhalation delivery |
|Adverse effects |Can trigger bronchospasm |
|Other |antidote for Tylenol |
Colds
• Drug regimen
– Symptomatic
– Combination products
• Decongestants
• Antitussives
• Analgesics
• Antihistamines - anticholinergic to suppress mucus
• Caffeine
Ch. 17 Treatment of Severe Allergy
Adrenergic Agonist
|Epinephrine |
|MOA/ Use |Direct receptor binding (( 1&2, (1&2) mimicing the sympathetic nervous system |
| |Also known as sympathomimetic & catecholamine |
|ADME |Broken down quickly in stomach & significant 1st pass effect (can’t take by mouth) |
| |Can’t cross blood-brain |
| |Discolors (pink/brownish) as it degrades (If, then?) |
|TE |Vasoconstriction (most common use) |
| |Hemostasis |
| |Augments local anesthetic via vascontriction |
| |Elevates blood pressure |
| |Restores beating heart |
| |Bronchodilates |
| |TOC for anaphylactic shock |
| |Mydriasis (rare use) |
|Adverse effects |HTN, necrosis, bradycardia w/ HTN, tachycardia, tremor, chest pain, elevated blood sugar |
|D ( D |MAOIs |
| |TCAs |
| |General anesthestics (myocardial effects) |
|Precautions |IV admin can cause potentially fatal effect – check concentrations! |
| |Insure patent and healthy IV site |
|EpiPen |Anaphylactic deaths |
| |PCN, venoms & foods |
| |Device: EpiPen & EpiPen Jr. |
| |Storage & Replacement |
| |Room temp – dark – do NOT refrigerate |
| |Injection |
| |Dose dependant on weight |
| |Duration |
| |Around 20 min and monitor for 6 hours |
| |SEs- heart rate increase |
Ch. 76 Selected Drugs for Peptic Ulcer Disease (PUD)
Histamine2 – Receptor Antagonists
|Cemetadine (Tagamet) |
|First choice for gastric / duodenal ulcers |
|MAO/ Use |Promote healing through acid reduction |
| | |
| |GERD, Aspiration Pneumonitis in obese & gyne prior to anesthesia |
|Adverse effects |Low incidence of gynecomastia, reduced libido, impotence, CNS depression / excitement, pneumonia |
|D ( D |Inhibits hepatic drug metabolism – therefore? |
| |Major Drugs of concern – warfarin, phenytoin, theophylline, lidocaine |
Table 76-1 (use for histamine and rest of outline)
Famotadine (Pepcid)
• For heartburn, acid indigestion, sour stomach
• Cut dose in renal compromise/ failure
• No antiandrogenic effects
• No effect on hepatic metabolism of other drugs
Proton Pump Inhibitors
|Omeprazole (Prilosec) |
|MOA/ Uses |suppress secretion of gastric acid |
| |Irreversible - days - up to weeks after cessation |
| |Superior to H2RAs |
|Adverse effects |HA, diarrhea, N & V |
| |Long term may increase risk of CA |
|ADME |give 30 min before meal – once daily |
|D(D, D(F |Reduced absorption of atazanavir, ketocanazole and itracanazole – NOT recommended concurrently with atazanavir |
Antacids
|Magnesium hydroxide/ Aluminum hydroxide |
|MOA/ Uses |alkaline agents that neutralize acid & decrease destruction of gut wall |
| |And prophylactically to prevent aspiration pneumonia |
|ADME | Take regularly to promote healing |
| |In PUD: 1 and 3 hr after each meal & at bedtime |
| |Goal is gastric pH greater than 5 |
|Adverse effects |Constipation (aluminum base) / Diarrhea (magnesium base) |
| |Sodium “loading” |
| |High levels in renal failure clients |
|D(D |May interfere with absorption of other drugs |
................
................
In order to avoid copyright disputes, this page is only a partial summary.
To fulfill the demand for quickly locating and searching documents.
It is intelligent file search solution for home and business.
Related searches
- world history unit 2 vocabulary
- physics unit 2 test
- american government unit 2 quizlet
- government unit 2 quizlet
- entrepreneurship unit 2 ia
- biology unit 2 test answers
- biology unit 2 assessment
- unit 2 test review answers
- unit 2 test review biology
- unit 2 biology practice test
- unit 2 test review math
- unit 2 geometry test answers