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Pharm exam two
| Question | Answer |
|---|---|
| Seizure | Brief episode of abnormal electrical activity in the nerve cells of the brain |
| Convulsion | Involuntary spasmodic contractions of any or all voluntary muscles throughout the body, including skeletal, facial and ocular muscles |
| Epilepsy | Chronic, recurrent pattern of seizures |
| Primary (idiopathic) | Cause cannot be determined |
| Secondary | Distinct cause identified |
| Partial seizures | short alterations in consciousness Repetitive unusual movements Psychologic changes confusion |
| Generalized seizures | Temp. lapses of consciousness (stares off in space, daydreaming, and inattentive look) Rhythmic movements of eyes, head or hands Occurs several times/day |
| Status Seizure | Generalized tonic-clonic convulsions that occur in succession |
| Febrile Seizure | occur b/n 6 mos. And 5 yrs. caused by fever. They outgrow these and it’s usu. Tx by Tylenol |
| Simple Seizure | Spasms of a muscles Effects one part of body Does not effect LOC |
| Complex Partial Seizure | Involves temporal Lobes Consciousness impaired Aura experience Random purposeful movement, confused |
| AED (anti-epileptic drugs) | If 2nd med. Is needed, taper 1st while ↑ 2nd. Never abruptly stop AED! |
| Mechanism of Action- Anitepileptic | Prevent spread of excessive electrical discharge from abnormally functioning nerve cells Protect surrounding normal cells; Neurons are stabilized Neuron hyperexcitability is ↓ The spread of excessive nerve impulses is ↓ |
| Phenobarbital (Solfoton) | Has longest half-life. Will only be given once a day. Very sedating. Children may show s/s of irritability/hyperactivity Toxicity – nystagmus, ataxia, resp. ↓, ↓ b/p, coma |
| ***Diazepam (Valium)*** | DOC for status epilpticus |
| Carbamazepine (Tegretol) | autoinduction occurs drug ↑ its own metabolism over time ↓ drug concentrations. Begin with low dose and gradually ↑. Can cause blood dyscrasias Avoid grapefruit juice (inhibits metabolism ↑ carbamazepine levels Monitor Na+ levels edema MonWarfa |
| Hydantoins -phenytoin (Dilantin) | Has ↑ adverse effect: sedation, gingival hyperplasia, skin rash, dysrhythmias, ↓ b/p, hirsutism, alteration in vitamin D metabolism ↓ effects of oral contraceptives, warfarin, and glucocorticoids if taken together |
| Valproic acid (Depakote) | Has ↑ adverse effect: GI - n/v/indigestion; hepatotoxicity (monitor liver enzymes) anorexia, abd. pain, jaundice; pancreatitis - (monitor amylase levels); thrombocytopenia (monitor plt. count) Use carefully with phenobarbital (↑ levels of both drugs) |
| Topiramate (Topamax) | Should force fluids to avoid renal calculi b. Should use a backup contraception Given in regular-release capsule (can open and sprinkle on small amt. of soft food |
| Parkinson’s Disease (PD) | Chronic, progressive, degenerative disorder Affects the dopamine-producing neurons in the brain Caused by an imbalance of two neurotransmitters within this part of the brain Dopamine – inhibitory Acetylcholine (ACh) – excitory |
| Classic symptoms: (Parkinson's) | Akinesia – no movement Bradykinesia – slowness Postural instability – difficulty in walking. (start/stop) Rigidity – “Cogwheel” rigidity – resistance to passive movement Tremors – decreases with voluntary movement; 70 % of cases |
| Levodopa | (converts to dopamine) On-off phenomenon - Rapid swings in response to levodopa occur |
| Amantadine (Symmetrel) | ↑ release of dopamine at the end of nerve cells (presynaptic) blocks the reuptake of dopamine into the nerve endings→↑ in synapse for dopaminergic receptors Does not stimulate dopamine receptors directly (prevents reuptake) Also has antiviral effects |
| Ergot Bromocriptine (Parlodel) | Directly stimulates the dopamine receptors (activates dopamine receptors → ↑ dopamine production) |
| Nonergot Ropinirole (Requip) | Same as above with fewer dyskinesias effects. Used for PD & restless leg syndrome |
| Analgesics | Narcotics NSAIDs Antimigraine agents |
| Pain | it whatever the patient says it is and occurs whenever the patient says it exists It’s an unpleasant sensory and emotional experience associated with actual or potential tissue damage Involves physical, psychological & emotional factors |
| Perception (nociception) | The awareness of the feeling or sensation of pain |
| Threshold | The point at which a person 1st acknowledges or interprets the sensation of “pain” |
| Tolerance | The amount of pain a patient can endure without it interfering with normal function (becomes unbearable) |
| Lowered: threshold of pain | Anger, anxiety, depression, discomfort, fear, isolated, chronic pain, sleeplessness, tiredness |
| Raised: threshold of pain | Diversion, empathy/sympathy, rest, drugs (analgesics, antianxiety, antidepressants) |
| Acute pain | Sudden in onset (mins – hrs) -Intensity is proportional to extent of tissue damage -SNS is activated: ↑HR, ↑BP, diaphoresis, pallor -Subsides once treated/healing -Under (6 weeks) 3 months |
| Chronic pain | Slow onset and persistent Lasting > 3 mon Often difficult to treat Dull, persistent ache Can affect almost every aspect of patient's life (physical, mental, social, financial, & spiritual) Frequently causes stress, anger, chronic fatigue, & depres |
| Somatic | originates skeletal muscles, ligaments & joints |
| Visceral | originates organs & smooth muscle |
| Superficial | originates skin & mucus membranes |
| Vascular | vascular or perivascular (migraines) |
| Referred | when visceral nerve fibers are close to sub-q fibers in the spinal cord |
| Neuropathic | damage peripheral or CNS nerve fibers injured or diseases or idiopathic |
| Phantom | surgical or traumatic removal of body part (paralyzed limbs from spinal cord injury) burning, itching, tingling, stabbing. |
| Cancer | caused by pressure of tumor, hypoxia, metastases, fractures, muscles spasms, radiation, chemo. Etc |
| Central | tumors, trauma, inflamm or disease affecting CNS tissues |
| Neurotransmitters Glutamate | this seems to be the dominant neurotransmitter when the threshold to pain is first crossed, → acute pain. |
| Substance P | this is a peptide and is released by C fibers. It is generally associated with intense, persistent, chronic pain, and used to relay pain messages leading to the spinal cord and brain |
| Pain Transmission Gate Theory | Pain fibers enter spinal cord via dorsal horn (gate) & travel to brain for pain interpretation |
| gate theory | Activation of large diameter “A” fibers closes gate → inhibits transmission to brain & limits perception of pain |
| C Fibers | Activation of small diameter “C” fibers opens gate → permits impulse transmission → pain |
| Body has endogenous neurotransmitters | Enkephalins Endorphins “endogenous mophine” Produced by body to fight pain Bind to opioid receptors → ↓transmission of pain by closing gate |
| Opioid Receptors | 5 types of opioid receptors within CNS →control pain. When blocked by opiates→ Ø pain Mu *, Kappa *, Delta * * Primary receptors Sigma & Epsilon |
| Agonist | bind to opioid pain receptor in brain → analgesic response (↓ severe pain) |
| Partial agonist | - bind to a pain receptor → Treats mild to moderate pain ( Ø severe) (Also called agonist-antagonists or mixed agonist) (Stadol) |
| Antagonist | – (reversal effects) bind to pain receptor → no response (Also called competitive antagonists) |
| Physical Dependence: | physiologic adaptation of the body to the presence of an opioid. (agitation, tachycardia, HTN, seizure) |
| Psychological Dependence: | pattern of compulsive drug use characterized by a continued craving for an opioid and the need to use the opioid for effects other than pain relief |
| Opioid withdrawal/Opioid abstinence syndrome | –abrupt cessation, rapid dose reduction, antagonist administered. (anxiety, chills, joint pain, rhinorrhea, diaphoresis, N/V, abdominal cramps, confusion, etc. pg 157) |
| Adjuvant drug therapy | – combination of opioid drugs with other chemical drugs (antidepressants, NSAIDS, anticonvulsants, corticosteroids to help control pain. Usu. Opioid dose is smaller. Creates a synergistic effect |
| Analgesic Ceiling Effect | once a specific dosage is reached, the drug produces a maximal analgesic effect. If dosage ↑, pain will not improve, but adverse effects ↑ (Stadol) |
| Adverse Effects: opiods | euphoria, sedation, lightheadedness, ↓seizure threshold, tremors CV: ↓ b/p, palpitation, flushing respiratory depression & aggravation of asthma n/v, constipation, biliary tract spasm (stim. CNS n/v control centers) urinary retention (↑ bladder tone) |
| *All opioids release histamine | → itching, rash, (vasodilation) flushing, ↓ b/p , etc. |
| Contraindications: for opiods | Known drug allergy Severe asthma or other respiratory insufficiency Morbid obesity/sleep apnea Paralytic ileus Elevated intracranial pressure Pregnancy |
| Nonopioid Analgesics: Acetaminophen- Tylenol | Mild-mod pain,fever,alternative to aspirin DOC 4→Reye’s syn Blocks pain impulses inhibit prostaglandin synthesis fever by acting on hypothalamus (regof temp) Max 4000mg/d Doesnt have antiinflammatory effects Does not have unwanted effects of NSIAD |
| Toxicity & Managing Overdose of acetaminophen | Recommended antidote: acetylcysteine Dangerous interactions with alcohol, hepatotoxic drugs Contraindication: liver disease, G6PD deficiency-genetic disease ADR: rash, N/V, blood disorders, hepatotoxicity |
| Perform a thorough pain assessment: 5th vital sign | Character: s/s Onset Location Duration Severity (0 – 10 scale) Pattern: aggravating and alleviating factors Associated factors: What other symptoms have occurred? |
| AIDS | Caused by HIV, weakens immune system |
| Antibodies | imminoglobulin molecules that attack and destroy antigen |
| Antigen | foreign to host that causes some sort of sickness |
| Antiretroviral drug | works against retro viruses like hiv |
| antiviral drugs | drug used to destroy viruses |
| cell mediated immunity | nonspecific T cells and monocytes, macro, neutrophils |
| dna | a self-replicating material present in nearly all living organisms as the main constituent of chromosomes. It is the carrier of genetic information. |
| fusion | viruses attach themselves to host |
| genome | complete set of genetic info |
| herpesviruses | viruses that cause herpes |
| host | organism that is infected with bacteria or viruses |
| HIV | retro virus that causes AIDs; human immunodeficiency virus |
| humoral immunity | B lymphocytes |
| immunoglobulins | use to attack and kill antigens |
| Influenza viruses | viral infrections in resp tract. A,B,C types only meds to treat A & B at time |
| herpes 1 | fever blisters, cold sores |
| herpes 2 | genital herpes |
| herpes 3 | chicken pox, shingles |
| herpes 4 | epstein barr "mono" |
| Herpes 5 | cmv eye infection |
| herpes 6-7 | infections in hiv |
| herpes 8 | kapsi sarcoma |
| Antiviral | MOA: blocks activity of polymerase enzyme that stimulates the synthesis of viral genomes.impaired viral replication; contraindication- allergies ADR- Seizures, renal failure, SJ syndrome, Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome |
| ****Acyclovir (Zovirax) | antiviral; treats herpes types 1&2 chickenpoxs PO, topical, IM |
| *****Ganicilovir (Cytovene) | treatment of infections caused by CMV |
| ****Non hiv drugs | acyclovir, amantadine, ganciclovir, ribavirin |
| HIV drugs | indinavir, nevirapine, tenoforvir, maraviroc, raltegravir, zidovudine |
| Stages of HIV | 1) symptomatic infection 2) early general symptoms of dx 3) moderate symptoms 4) severe symptoms |
| indinavir | protease inhibitor PO only |
| neviraoine | NNRTI (non nucleoside reverse transcriptase inhibitors) |
| zidovudine | aziddothymidine or AZT synthetic nucleoside analogue of thymidine; Retrovir; PO; 6 months for therapeutic effect; 0.8-2 hr half life; 3-5 hr duration of action |
| aerobic | requires O2 |
| anti-TB drug | drugs used to infections caused by mycobacterium bacteria ADR- flu symptoms;joint pain or edema; easy bruising or bleeding urinating less than usual or not at all; ornausea, stomach pain, loss of appetite, itching, clay-colored stools, jaundice |
| bacillus | rod shaped |
| granulomas | small nodular aggregations of inflammatory cells |
| MDR-TB | tb that is resistance to 2 or more drugs |
| slow acetylator | genetic defect that causes a deficiency in the enzyme needed to metabolize isoniazid |
| Tubercle | small round gray granulomatous lesion with a cheesy consistency |
| TB | an infectious bacterial disease characterized by the growth of nodules (tubercles) in the tissues, esp. the lungs. The disease is caused by the bacterium Mycobacterium tuberculosis; Gram-positive acid-fast rods |
| Diagnosis of TB | 1) PPD (MANTOUX TEST) 2) if skin test is + then chest xray 3) if chest xray shows signs of tb then culture of sputum |
| *****first line drugs | ethambutol, isoniazid, pyrazinamide, rifabutin, rifampin, rifapentine, streptomycin |
| 2nd line drugs | amikacin, capreomycin, cycloserine, ehtionamide, kamamycin, levofloxacin, oflozacin, para-aminosalucylic acid |
| vit b6 | needed to combat peripheral neuropathy associated w. isoniazid |
| *****Rifampin | reddish brown urine/ other body fluids antitubercular contraindication- allergies, other amprenavir |
| when is one contagious with TB? | during the initial period of the illness and its diagnosis |
| liver toxicity in TB pt | darkened urine, fatigue, jaundice |
| Antimetabolite | a drug or other substance that is a receptor antagonist or resembles a normal function by competing |
| dermatophyte | fungi that is found in soil, infects skin, nails, or hair. |
| ergosterol | yeast, mushrooms, ergot, main sterol in fungal membranes |
| fungi | external carbon (yeast molds) |
| molds | long branching filaments called hyphae |
| mycosis | any fungal infection |
| pathologic fungi | fungi that causes mycoses |
| sterols | polyene antifungal drugs bind too |
| yeasts | single cell that reproduces by budding |
| *****amphotericin B | DOC (chills, fevers, n/v, HA) pretreatment of anitpyretic, antihistamines, and antiemetics |
| fluconazole | excellent bioavailability |
| oral candidiasis | thrush |
| caspofungin | blood dyscrasias, hypotension, hepatotoxicity |
| ***anthelmintic | drug that destroys or prevents the dev. of parasitic worms |
| antimalaria drugs | drugs that destroy or prevent malaria parasite |
| antiprotozoal | drugs that destory or prevent dev. of protozoans ADR- flu,infection sx;Black, tarry stools; Blood in urine or stools; Pinpoint red spots on the skin; weakness. contra-allergies, psoriasis, retinal disorders, epilepsey MOA- inhibit protein synthesis |
| helminthic infections | parasitic worm infections |
| malaria | infectious dx caused by plasmodium |
| parasite | organism that feeds off another organism causing harm in the host |
| parasitic protozoans | parasites that live off organisms while causing a harmful dx in the process |
| protozoans | single celled that are the smallest and simplest members of the animal kingdom |
| chloroquine & hydroxchoroquine | synthetic antimalarial, (changes in visual field, optic nerves, psoriasis) also used to treat rheumatoid arthritis |
| primaquine | 8 aminoquinoline (destroys the malarial parasites while they are in the exoerythrocytic phase (tissue phase) |
| metronidazole | treatment of trichomoniasis, amebiasis, and giardiasis to the treatment of anaerobic infections and antibiotic induced pseudomembranous colitis give c food, infusing iv does over 30-60 min, obtain ordered specimens before starting meds. |
| when administering antiprotozoal drugs review what base line | hemoglobin levels |
| indinavir | Crixivan; antiretroviral; PO, 2 wk therapeutic effect, 1.5-2.5 hr half life, 6 month duration of action; recommend fasting |
| nevirapine | Viramune; PO 2 hr onset, 25-30 hr half life; 24 hr duration of action; for HIV infection- well tolerated; adverse- rash, fever, nausea, HA, abnormal liver function test |
| *** isoniazid | INH; primary/ most used anti-TB drug; adverse- drug-induced hepatitis; peripheral neuropathy time- rapid; 1-2 hrs drug-drug interactions- additive CNS toxicity; BCG vaccine (not effective) contraindications- allergies, acute liver disease |
| amphotericin B | antifungal adverse effects- chest pain, hypotension, NVD, nephrotoxicity, increased liver enzymes, hyperbilirubinemia, chills, fever nursing interaction w/ ADR- vitals, injection site, intake/output contraindications- allergies, lactation |
| hydroxychloroquine | antimalarials & antiheumatics inhibits protein synthesis- inhibit DNA/RNA polymerase PO, 4 hr onset, 32-50 day half life, variable duration |
| metronidazole | antiprotozoal; broad antibacterial/anthelmintic activity; treat trichomoniasis, amebiasis, giardiasis, treat anaerobic bacterial infections and antibiotic induced pseudomembranous colitis PO, 3 hrs onset of action, 8 hr half life, variable duration of ac |
| chloroquine | antimalarial, treat- parasitic infection PO, 8-10 hr onset, 3-5 day half life, variable duration |
| ***** mebendazole | antihelmintics- treatment of many kinds of round worms and a few types of tape worms adverse effects- seizures, HA, dizziness, tinnitus, ABD pain, NVD, rash, alopecia, numbness, fever, leukopenia, thrombocytopenia |
| Start low | and go slow |
| Medications should be directed to Target Symptoms | what seems to be the major issues… sleep etc etc etc |
| Attempt to avoid | polypharmacy |
| Psychosis | Severe emotional disorder impairs mental function of affected individual to point that individual cannot participate in activities of daily living (what’s real and what’s not real) |
| Mood Disorders | Changes in mood ranges from mania (abnormally increased emotions) to depression (abnormally reduced emotions) Some patients may exhibit both mania and depression: bipolar disorder (BPD) |
| Anxiety (def) | Unpleasant state of mind, characterized by a sense of dread and fear May be based on actual anticipated experiences or past experiences May be exaggerated responses to imaginary negative situations |
| Anxiety (types) | Obsessive-compulsive disorder (OCD) Posttraumatic stress disorder (PTSD) Generalized anxiety disorder (GAD) Panic disorder Social phobia Simple phobia |
| Psychotherapeutics: Pathophysiology | Biochemical imbalance theory Mental disorders are associated with abnormal levels of endogenous chemicals, such as brain neurotransmitters |
| Biochemical imbalance theory | Catecholamines Dopamine (schizophrenia too much) Norepinephrine (depression low levels) Indolamines Serotonin (depression low levels) Histamine (alertness to much to energitic, to much worry) Benadryl |
| Other bio-chemicals necessary for normal mental function | GABA ( calms us down inhibitory of stress) Acetylcholine (ACh) Glutamate/NMDA receptor (tends to be excitatory) might cause Alzheimer's |
| dopaminergic pathways | Mesolimbic (emotional ) Mesocortical (brain) Nigrostriatal (basal ganglia) (schizophrenia) Tuberoinfundibular- (hyopthalmus and pituitary gland) Thalamic |
| Antianxiety Drugs | All reduce anxiety by reducing overactivity in the CNS |
| MAOI | Highly effective Considered second-line treatment for depression unresponsive to cyclics Disadvantage: potential to cause hypertensive crisis when taken with tyramine phenelzine (Nardil) tranylcypromine (Parnate) |
| MAOIs & SSRIs | may lead to serotonin syndrome If the decision is made to switch to an SSRI, there must be a 2- to 5-week “wash-out” period between MAOI therapy and SSRI therapy |
| SSRI | fluoxetine (Prozac) paroxetine (Paxil) sertraline (Zoloft) fluvoxamine (Luvox) citalopram (Celexa) escitalopram (Lexapro) |
| SSRI (MOA) | Selectively inhibit serotonin reuptake Little or no effect on norepinephrine or dopamine reuptake Result in increased serotonin concentrations at nerve endings Advantage over tricyclics and MAOIs: little or no effect on CV system |
| Tricyclic antidepressant- first generation | Largely replaced as first-line antidepressant drugs by SSRIs Second-line For patients who fail with SSRIs or other newer-generation antidepressants As adjunct therapy with newer antidepressants |
| Tricyclic antidepressant- common drugs | amitriptyline (Elavil, Endep) (HA BACK PAIN, 25-50 MG BUT FOR DEPRESSION HIGH DOSE) doxepin (Sinequan) imipramine (Tofranil) desipramine (Norpramin) nortriptyline (Aventyl, Pamelor) |
| Tricyclic antidepressant- MOA | Block reuptake of neurotransmitters, causing accumulation at the nerve endings It is thought that increasing concentrations of neurotransmitters will correct the abnormally low levels that lead to depression |
| Tricyclic antidepressant- side effects | Blockade of norepinephrine reuptake Antidepressant,* tremors, tachycardia, others Blockade of serotonin reuptake Antidepressant,* nausea, headache, anxiety, sexual dysfunction *Desired therapeutic effects |
| Tricyclic antidepressant- indications | Depression Childhood enuresis (imipramine) Obsessive-compulsive disorders (clomipramine) Adjunctive analgesics for chronic pain conditions, such as trigeminal neuralgia, ha, fibermyalgia |
| Tricyclic antidepressant- adverse | Sedation Impotence Orthostatic hypotension, Older patients- Dizziness, postural hypotension, constipation, delayed micturation, edema, muscle tremors Anticholengeric Tachycardia, Suicide potential Bad seizures |
| Tricyclic antidepressant- OD | 70% to 80% die before reaching the hospital CNS and cardiovascular systems are mainly affected Death results from seizures or dysrhythmias |
| Tricyclic antidepressant- OD cont'd | No specific antidote Decrease drug absorption with activated charcoal Speed elimination by alkalinizing urine Manage seizures and dysrhythmias |
| Risperidone | antipsychotic |
| Haldol | Butyrophenones/ antipsychotics haloperidol |
| Lithium | mood stabilizer/ antimanic |
| Prozac | SSRI |
| Nardil | MAOI |
| Thorazine | chlorpromazine; type of antipsychotic, Phenothiazines |
| Amitriptyline | tricyclic |
| Clozaril | atypical antipscyhotics; second generation antipsychotics |
| Wellbutrin | second generation antipsychotics |
| Antibiotics | Medications used to treat bacterial infections Bactericidal: kill bacteria Bacteriostatic: inhibit growth of susceptible bacteria → will eventually lead to death |
| Gram Negative | is usually hard to cure- b/c of lipid layer |
| Empiric therapy: | obtaining culture before treatment |
| Definitive therapy: | tx w/ Abx. while obtaining specimen (sputum). Then tailoring the Abx. to the specimen identified. |
| Prophylactic therapy | tx w/ Abx. to prevent an infection, as in intraabdominal surgery or after trauma |
| Therapeutic response: | ↓ S/S of infection (fever, ↑ WBC, redness, inflammation, drainage, pain) |
| Subtherapeutic response | S/S of infection do not improve. Causes: incorrect route or dose of Abx., inadequate drainage of abscess, poor penetration of drug to infection, bacterial resistance to drug |
| Superinfection | bacteria/fungi are killed → allowing other bacteria/fungi to grow (vaginal yeast infection) |
| Superinfection | bacteria/fungi are killed → allowing other bacteria/fungi to grow (vaginal yeast infection) |
| Pseudomembranous colitis | Abx frequently causes diarrhea (ADR) It may cause a Abx.-associated colitis b/c Abx. Disrupt normal gut flora and can cause overgrowth of Clostridium difficile. S/s of C. difficile: watery diarrhea, abd. Pain, and fever. Now need to tx C. difficile |
| Antibiotic resistance | causes over prescribed Abx., not completing prescriptions, etc. |
| Drug-drug and drug-food interactions | common problems Tetracycline (Nausea) (messes w/ ca) & milk - absorption Quinolones & antacids or MVI with iron absorption |
| Antibiotics: Classes | Sulfonamides Penicillins Cephalosporins Tetracyclines Aminoglycosides Quinolones Macrolides Others |
| 4 MOA for Abx: | Interference w/ cell wall synthesis penetrate & destroy cell wall permits high oncotic pressure inside cell which draw fluid into cell Cell fills & burst Interference w/ protein synthesis |
| 4 MOA for Abx: con't | Interference with DNA/RNA replication Acting as a metabolite to disrupt critical metabolic reactions inside the bacterial cell |
| H influenza | aka Meningitis treated with Cephalosporins (MOA, therapeutic/ adverse effects same as penicillins); ceftriaxone (Rocephin)Crosses Blood-brain barrier; 96% bind to protein; Don’t give w/ hepatic failure; meropenem (Merrem)- (Carbapenems)-tx bacterial ONL |
| Foscavir | antiviral; AIDS pt w. CMV MOA- Viral DNA Polymerase Inhibitor ADR- polyuria, polydypsia, spasms, flu symptoms, seizure, weak, nephrotoxicity contra- allergies |
| Antifungal therapy | drugs are used to treat infections caused by fungi and to prevent the development of fungal infections in patients with weakened immune systems.- nystatin, amphotericin B, difulcan, Nizoral, cancidas,sporanox |
| Diflucan | antifungal; for infections caused by susceptible organisms (ex. UTI) MOA- inhibit fungal sterols ADR- hepatotoxicity, SJ syndrome |
| Nystatin | antifungals; treat diaper rash adverse effects- NVD, contact dermatitis nursing interaction w/ ADR- inspect mucous membranes |
| Lamisil | antifungal; for fungus on toenails/fingernails; ADR- burning, itching, local allergic rxn, red, stinging contra- allergies MOA- affect synthesis of fungal cell wall |
| Malaria | parasitic disease; high fevers, shaking chills, flu-like symptoms, and anemia; malaria drugs given PO which drugs- hydroxychloroquine, chloroquine, mefloquine, primaquine, pyrimethamine |
| Antifungals | adverse effects- chest pain, hypotension, NVD, nephrotoxicity, increased liver enzymes, hyperbilirubinemia, chills, fever nursing interaction w/ ADR- vitals, injection site, intake/output contraindications- allergies, lactation |
| exoerythrocytic phase of malaria | tissue phase (in liver)-->blood-->second vector-->next human |
| Sulfamethoxazole/trimethoprim – SMX-TMP (Bactrim - co-trimoxazole)- Abx | Bacteriostatic action Prevent synthesis of folic acid needed for synthesis DNA/RNA interferes w/ metabolism of bacteria eventually kill it Only affect MO that synthesize own folic acid no affect human cells/certain bacteria that use exogenous folic acid |
| Sulfonamides: Indications | UTI caused by Enterobacter species, Ecoli, Klebsiella Proteus mirabilis, Proteus vulgaris,Staphylococcus aureus Respiratory Infections Pneumocystis jiroveci pneumonia (PJP) URT-now less effective against strept Otitis media Common tx with outpt. MRSA |
| Sulfonamides: ADR most common | Photosensitivity, Allergic reaction |
| Sulfonamides: ADR | Hemolytic and aplastic anemia,agranulocytosis, thrombocytopenia dermatitis, Stevens-Johnson syndrome, epidermal necrolysis N/V/D, pancreatitis, hepatotoxicity Convulsions, crystalluria, toxic nephrosis,HA, cough, pulmonary infiltrates,peripheral neuritis |
| β-Lactam Antibiotics | beta-lactam ring- part of their chemical structure Bacterial became resistant by forming beta-lactamase, an enzyme that attacks the beta-lactum ring decr.efficacy of antibiotics Beta-lactamase inhibitors prevents B-lactamase from producing emzyme |
| Penicillins (β-lactams) | These chemicals bind with β-lactamase and prevent the enzyme from breaking down the penicillin, thus making the drug more effective: Clavulanic acid, Tazobactam, Sulbactam |
| Penicillins- Contraindication | known drug allergies. If allergic to PCN → 4–6x > allergic to other β-lactam antibiotics, especially cephalosporins |
| Penicillins ADR | Lethargy, hallucinations, anxiety, depression, twitching, coma, seizures, NVS abd pain, colitis, thrush, anemia, increased bleed time, bone marrow depression, granulocytopenia, hyperkalemia, hypokalemia, alkalosis, hives, rash, prutitus |
| Cephalosporins | related to penicillins Identical MOA,therapeutic/adverse effects Nephrotoxicity possible, if taking w/aminoglycosides Bactericidal & Broad spectrum Used surgical prophylaxis, URIs, otitis media,UTI,abd. infec bacteremia meningitis & osteomyelitis |
| Cephalosporins- 1st generation | First Generation: Cephalexin (keflex, biocef) Only in po form Cefadroxil Indications: Good gram-positive coverage & poor gram-negative Used for surgical prophylaxis, URIs, otitis media |
| Cephalosporins- 2nd generation | Good Gram + Better Gram -coverage than 1st gen. cefaclor cefuroxime (Ceftin, Zinacef) –surgical prophylaxis & doesn’t kill anaerobes loracarbef cefotetan cefprozil Cefoxitin (Mefoxin) used prophylactically for abd./colorectal surgeries. Kills anaerobes |
| Cephalosporins- 3rd generation | Indications: most potent group against Gram – coverage; < active Gram + cefotaxime cefpodoxime ceftibuten cefdinir |
| Cephalosporins- 4th generation | Broader spectrum > 3rd Gen., esp. w/ Gram + . Covers both Gr – & Gr + cefepime (Maxipime) Good against Enterobacter spp (Gr -) & Gr + UTI, skin infections, and pneumonia IV or IM only |
| Cephalosporins- 5th generation | ceftobiprole (not yet marketed) Newest cephalosporin drugs Effective against MRSA, Pseudomonas spp. IV only |
| Carbapenems | Broadest antibacterial antibiotics. Gr + & Gr. – Aaerobic/anaerobic bacteria Bactericidal & inhibit cell wall synthesis Can induce seizure activity – rare. Usu in elderly & renal pt. not adm. if pts has PCN anaphylactic reactions Given over 60 mins |
| Monobactams | aztreonam (Azactam) Synthetic β-lactam antibiotic Primarily against aerobic Gram - bacteria (E. coli, Klebsiella,pseudomonas) used severe systemic infections & UTI advantage - it preserves normal Gram + & anaerobic flora, unlike many β-lactam antibiotics |
| Macrolides-MOA | Prevent protein synthesis within bacterial cells Bacteriostatic & in ↑ concentrations → bactericidal These drugs are highly protein-bound and will cause severe interactions with other protein-bound drugs normal albumin levels!!!!!!!!!!!!!!!!!!!!!!! |
| MacrolideS-Indications | Strep infections (Streptococcus pyogenes) (group A β-hemolytic streptococci) Mild to moderate URI & LRI (Haemophilus influenzae) Spirochetal infections (Syphilis & Lyme disease) Gonorrhea, Chlamydia, Mycoplasma |
| Ketolide | Telithromycin (Ketek) Only drug in this class Better antibacterial coverage than macrolides Active against Gram + (including multi-drug resistant strains S. pneumoniae & selected Gram - bacteria Associated w/ severe liver damage & now very limited in use |
| Tetracyclines | Bacteriostatic → inhibit bacterial growth by inhibit protein synthesis Broad Spectrum: Gram - & Gram +, protozoa, mycoplasma, rickettsia, chlamydia, syphilis, Lyme disease (spirochetal infections), acne |
| Tetracycline drugs | Doxycycline (Doryx)Tx rickettsial chlamydial&mycoplasmal,spirochetal/Gr– infections Tigecycline (Tygacil) skin/soft tissue,intraabd.infections pneumonia.Effective against resistant bacteria Demeclocycline(Declomycin) tx for SIADH(syndrome inapprop. ADH |
| Tetracycline nursing interventions | → do not take with dairy products, antacids, & iron salts → ↓ oral absorption Take with 6 - 8 oz water Photosensitivity → avoid sunlight & tanning beds |
| Tetracycline- ADR | binds to Ca & ↓ absorption teeth formation Discoloration tooth enamel in fetuses/children (< 8)nursing infants May retard fetal skeletal development Alter intestinal flora→ Superinfection,D,(c diff) Alter vag flora → Vaginal candidiasis Maculopapular ras |
| Multidrug resistance organisms | MRSA – methicillin resistant Staphylocccus aureus VRE– vancomycin resistant Enterococcus Usually UTI ESBL– extended-spectrum beta-lactamases tx w/carbapenems sometimes quinolones KPC – Klebseilla pneumoniae carbapenemase Tx w/ tigecycline & colistimetha |
| Minimum inhibitory concentration (MIC) | Lowest concentration to kill microorg. The serum levels should be 8 x higher than MIC |
| Time-dependent killing | amt. of time above MIC to kill microorg. |
| Concentration | dependent killing (aminoglycosides) higher more it will kill |
| Post-antibiotic effect (PAE) | after short-term abx tx, bacterial does not grow |
| Aminoglycosides | Poor oral absorption (except Neomycin – decontaminate GI tract before surgery)Very potent antibiotics with serious toxicities Bactericidal: prevents protein synthesis (binds to ribosomes) |
| Aminoglycosides con't | Pregnancy C & D. Cross the placenta fetal harm deafness).often used in combination w/ other antibiotics (beta-lactams or vanc) for synergistic effects. Very important – beta-lactam should be given 1st Once-daily vs. multi-daily 5 – 7 mg/kg/day |
| ****Aminoglycosides**** | **Ototoxicity and nephrotoxicity Headache *Paresthesia *Fever *Superinfections Vertigo *Skin rash *Dizziness Monitor peak and trough blood levels |
| Aminoglycosides- Drug interactions | Loop diuretics increasing ototoxicity Kills normal flora in GI decreasing Vit. K produced increasing warfarin levels Prolongs duration of neuromuscular blocking drugs |
| Aminoglycosdes- Nursing interventions: | Force fluids if possible (3000 mL/day) Teach to report ADR, esp. h/a, vertigo, and nausea Report s/s/ of superinfection: diarrhea, vaginal d/c, stomatitis, glottitis, hairy tongue, and cough |
| INDICAITONS: Serious Gram Negative & some Gram Positive | Gram Negative: Pseudomonas species Enterbacteriaceae (E. Coli, Proteus species, Klebseilla species, Serratia species) Gram Positive: Entercoccus S. aureus Streptococcal Bacterial endocarditis **TID with Gr. Pos. and never used alone |
| quinolones | Effective against gram-neg & some gram-pos. organisms Lower RTI, Bone/joint infections, Infectious diarrhea, UTI, Skin infections, STD, & Anthrax Mostly excreted in kidneys MOA: Bactericidal Alter DNA of bacteriadeath No affect human DNA |
| quinolones ADR | HA,dizzy, fatigue, depression,restless insomnia, seizure N/V/D/C, thrush, ↑AST & ALT, flatulence, heartburn, dysphagia, colitiis |
| quinolones ADR con't | Rash, pruritus, urticaria, flushing, photosensitivity (w/ lomefloxacin)fever, chills, blurred vision, tinnitus,ruptured tendons & tendonitis |
| quinolones | Ciprofloxacin (Cipro) (Nosocomial & UTI) Better than PCN, Cephalosporin,/aminoglycosides).PO IV Only quinolone in generic form, Good against Psuedomonas/some Strept |
| quinolones (con't) | Levofloxacin (Levaquin) (broad sinusitis, bronchitis, pneumonia, prolong QT intervals) Better than Cipro against Gr. +, Enterococcus and S. aureus Moxifloxacin – good against S. pneumoniae. MRSA & VRE can be resistant against it Norfloxacin – PO= *GUI |
| clindamycin (Cleocin) | Inhibit protein synthesis Tx bone,GU, intraabd,anaerobic pnsumonia& septicemia,soft tissue infections Contraindicate ulcerative colitis, enteritis,infants< 1month May cause C diff Avoid near eyes.Tx for vag infection – no sex during drug tx/adm.entire abx |
| linezolid (Zyvox) | New class: oxazolidinones Tx (VRE), hospital-acquired skin infections (MRSA & CAP) HTN if taken w/ vasopressions, serotonin syndrome if taken w/ SSRIs,&reactions if taken w/ tyramine Is used when vancomycin is ineffective ADR – HA, NVD, & decrease pl |
| Vancomycin | Destroys cell wall Tx for staph enterocolitis and antibiotic induced(C.dif) DOC: MRSA& other Gr+ bact. Po absorbed poorly –local GI effects monitor blood lvls prevent oto & nephrotox |
| Vancomycin Serum levels | Serum:p18 –50 mcg/mL T10– 20 mcg/mL Draw right before admin Infuse 60 –90 min |
| Vancomycin ADR | Red man syndrome rapid IV adm → ↓ b/p s/s→ Flushing/itching of head, neck, face, upper trunk Slow infusion. |
| Vancomycin nursing intervention | Ensure adequate hydration (2 L fluids/24 hr) if not contraindicated to prevent nephrotoxicity Use cautiously / renal pts., hearing loss, elderly and neonates |
| NSAID | Large and chemically diverse group of drugs with the following properties: Antiinflammatory – a protective mechanism stimulated by injury of tissues to destroy, dilute or wall off injurious agent and injured tissue. |
| Nsaid- MOA | : Arterial, venous and capillary dilation→↑ blood flow ↑ vascular permeability(gets thru blood vessels goes to tissues causes swelling) (attracts plasma proteins and leukocytes) |
| Types of NSAIDs | Antipyretic (high temps) , Antirheumatic (joint) , Analgesic (reg. pain) |
| Analgesia MOA | tx of headaches, mild to moderate pain, and inflammation Block the chemical activity of either or both COX enzymes (prostaglandin [PG] pathway) and lipoxygenase (leukotrienes LT pathway) limits the undesirable inflammatory effect of Prostaglandins |
| NSAIDs: Indications | Analgesia (mild - moderate)Antigout effects Antiinflammatory effects Antipyretic effects Relief of vascular HA Platelet inhibition (aspirin) Bone, joint & muscle pain Osteoarthritis Rheumatoid arthritis Juvenile rheumatoid arthritis Dysmenorrhea Fever |
| Salicylates MOA | Inhibit prostaglandins (PG) PG sensitize pain receptors → pain PG promote s/s → inflammation PG → ↑ Temperatures in brain Unlike pain meds - salicylates do not change LOC |
| Salicylates -ADRs: | gastritis & ulcers, n/v (take w/ 8 oz. glass of water) renal toxicity: incr sodium, fluid retained, oliguria, renal failure prolongs bleeding time CNS toxicity: salicylism (tinnitus, dizziness, ha, N&V, confusion), fever, respiratory & metabolic acidosi |
| NSAID ADR | Dyspepsia, heartburn, epigastric distress, nausea GI bleeding* Mucosal lesions* (erosions or ulcerations) Renal Reductions in creatinine clearance Acute tubular necrosis with renal failure Cardiovascular Noncardiogenic pulmonary edema |
| NSAIDs: Salicylate Toxicity Adults | Adults: tinnitus and hearing loss Also vision loss, fever, lethargy, confusion, n/v. Severe: resp. depression and coma |
| NSAID- salicylate Toxicity Children | hyperventilation → respiratory alkalosis CNS effects (lethargy or excitability) Metabolic acidosis & seizures Febrile, N & V |
| NSAID- salicylate Toxicity OD | serum levels exceed 40 to 60 mg/dL Tx: d/c drug, gastric lavage( pumping of stomach) w/ charcoal, F & E replacement , IV NaHCO3 (monitor bicarb level ) (↓ met. Acidosis), supportive symptoms & possibly dialysis. NO antidote |
| NSAIDs: Antigout Drugs | Gout: problem with uric acid metabolism ↓excretion of uric acid ↑ production of uric acid → hyperuricemia → Uric acid crystals (sharp, needlelike) are deposited in tissues and joints →pain |
| Anitgout Drugs | allopurinol (Zyloprim) - ↓ production of uric acid Colchicine - ↓ inflammatory response to urate crystals in joint tissue Take on empty stomach for better absorption, ↑ fluid intake Assess renal function → ↑ ARF & fatigue |
| Anitgout Drugs longterm | Take long term to prevent gout episodes probenecid (Benemid), sulfinpyrazone (Anturane) - ↑ excretion of uric acid in the urine |
| Cytotec | inhibits gastric acid secretions and stimulates mucous secretions. It helps prevent gastric ulcers . Usually taken with NSAIDS |
| PD other drugs | Anticholinergic drugs – block ACh Antihistamines Direct Acting Dopamine-receptor agonists Indirect Acting Dopamine-receptor agonists MAO-B inhibitor: selegiline COMT inhibitor: entacapone, tolcapone Miscellaneous drug: amantadine |
| Monoamine Oxidase Inhibitor (MAOI) | MAOs break down catecholamines (dopamine, norepi., epinephrine & serotonin ) in the CNS, primarily the brain Monoamine oxidase non-selective: MAO-A & MAO-B. MAO-A is in the placenta, liver, & GI tract MAO-B is in blood platelets & brain |
| MAOIs cause drug-food interaction with | Tyramine-containing foods (cheese, wine, beer yogart) → severe HTN** |
| COMT (catechol ortho-methyltransferase)inhibitors: | COMT is enzyme that catalyzes catecholamines in synapse Tolcapone (Tasmar) works centrally and peripherally. Need to monitor liver enzymes (hepatotoxic). Used only when other drugs fail Entacapone (Comtan) works only peripherally |
| Anticholinergic Therapy | Anticholinergics block effects of Ach (PD ↑ ACh) Used to tX muscle tremors & muscle rigidity ↑ cholinergic activity. Cogwheel rigidity (arm flex toward body/elbow extended) & pill-rolling fingers/head bobbing while at rest They do not relieve bradykinesi |
| Anticholinergic Therapy- Drugs used | Drugs used: benztropine mesylate (Cogentin), trihexyphenidyl (Artane), biperiden (Akineton), procyclidine (Kemadrin) |
| Anticholinergic Therapy: ADR | Drowsiness, confusion, disorientation Constipation, nausea, vomiting Urinary retention, pain on urination Blurred vision, dilated pupils, photophobia, dry skin Decreased salivation, dry mouth |
| Selegiline ADR | dizziness, dyskinesias, Nausea, syncope |
| Gabapentin (Neurontin) | chemical analogue of GABA Tx of partial seizures. ADR= dizziness, drowsiness, Nausea, ataxia, visual.speech changes, edema. |
| Which types of antiviral drugs are used to treat HIV infection | Nonnucleoside reverse transcriptase inhibitors Protease inhibitors Reverse transcriptase inhibitors Fusion inhibitors |
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