Antiviral Agents
Chapter 39
I Viruses
A. Viral replication
1. a virus cannot replicate on its own
2. it must attach to and enter a host cell
3. it then uses the host cell’s energy to synthesize protein, DNA and RNA
B. Viruses are difficult to kill because they live inside our cells
1. any drug that kills a virus may also kill our cells
C. Viral infections
1. a competent immune system is the best way to treat viruses
2. a well functioning immune system will eliminate or effectively destroy virus replication
D. Immunocompromised pts have frequent viral infections
1. CA pts, esp leukemia or lymphoma
2. transplant pts, due to pharmacologic therapy
3. AIDS pts, disease attacks immune system
II Antivirals
A. Viruses killed by current antiviral therapy (killed does not mean cured...suppressed)
1. cytomegalovirus (CMV)
2. hepatitis viruses
3. herpes viruses
4. HIV
5. influenza viruses
6. respiratory syncytial virus (RSV)
B. Key characteristics of anitviral drugs
1. able to enter the cells infected with virus
2. interfere with viral nucleic acid synthesis and/or regulation
3. some agents interfere with ability of virus to bind to cells
4. some agents stimulate the body’s immune system
C. Antiviral medications
1. Antiviral agents
a. used to treat infections caused by viruses other than HIV
2. antiretroviral agents
a. used to treat infections caused by HIV, the virus that causes AIDS
b. HAART (cocktail 10- 30 k/year)
i. highly active antiretroviral therapy
ii. includes at least 3 meds
iii. these meds work in different ways to reduce the viral load
c. side effects
i. numerous and vary with each agent
ii. drug therapy may need to be modified b/c of side effects
iii. goal is to find the regimen that will best control the infection with a tolerable side effect profile
iv. medication regimens change during the course of the illness
III Side effects (antivirals)
A. Zidovudine (given during labor to HIV pts)
1. bone marrow suppression
2. nausea
3. headache
4. foscarnet
5. headache, seizures, acute renal failure, nausea, vomiting, diarrhea, others
B. Ganciclovir
1. bone marrow toxicity
2. n/v, anorexia
IV HIV
A. Human immunodeficiency virus infection
B. ELISA (enzyme-linked immunosorbent assay)
1. detects HIV exposure based on presence of human antibodies to the virus in the blood
C. retrovirus
D. transmitted by:
1. sexual activity
2. intravenous drug use
3. perinatally from mother to child
E. 5 stages of HIV infection
1. primary infection
2. asymptomatic infection
3. persistent generalized lymphadenopathy
4. symptomatic stage
5. progression to full blown aids
V Opportunistic Infections
A. protozoal
1. toxoplasmosis of the brain, others
B. fungal
1. candiadiasis of the lungs, esophagus, trachea
2. PCP, others
C. Viral
1. CMV disease
2. HSV infection, others
D. Bacterial
1. various mycobacterial infections
E. Opportunistic neoplasias
1. Kaposi’s sarcoma
F. others
Friday, August 8, 2008
Antitubercular
Antitubercular Drugs
Chapter 40
I Tuberculosis
A. Caused by Mycobacterium tuberculosis
1. aerobic bacillus
2. passed from infected:
a. humans
b. cows (bovine)
c. birds (avian)
B. Common infection sites
1. lung (primary)
2. brain
3. bone
4. liver
5. kidney
C. infections
1. tubercle bacilli are conveyed by droplets
2. droplets are expelled by coughing or sneezing, then gain entry into the body by inhalation.
3. tubercle bacilli then spread to other body organs via blood and lymphatic systems
4. tubercle bacilli may become dormant, or walled off by calcified or fibrous tissue
II Antitubercular Agents *used in combination
A. First line
1. isoniazid (most frequently used)
2. ethambutol
3. pyrazinamide (PZA)
4. rafampin
5. streptomycin
B. second line agents (b/c of resistance)
1. capreomycin
2. cycloserine
3. ethionamide
4. kanamycin
5. para-aminosalicyclic acid (PAS)
III Mechanism of action (3 groups)
A. Protein wall synthesis inhibitors
1. streptomycin
2. kanamycin
3. capreomycin
4. rifampin
5. rifabutin
B. Cell wall synthesis inhibitors
1. cycloserine
2. ethionamide
3. isoniazid
a. drug of choice for TB
b. restistant strains of Mycobacterium emerging
c. metabolized in the liver through acetylation – watch for “slow acetylators”
d. used alone or in combination with other agents
e. indications
i. used for the prophylaxis or treatment of TB (for 6 months)
C. Other mechanisms of action
IV Antitubucular therapy
A. Effectiveness depends on:
1. type of infection
2. adequate dosing
3. sufficient duration of treatment
4. drug compliance
5. selection of an effective drug combination
6. resistance and compliance are a big problem
B. Problems
1. drug-resistant organisms
a. multidrug-resistant TB (MDR-TB)
2. drug toxicity
3. patient noncompliance
V Side Effects
A. INH (Isoniazid)
1. peripheral neuritis (inflammation of nerve endings)
2. hepatotoxicity
B. Ethambutol
1. retrobulbar neuritis
2. blindness
C. Rifampin
1. hepatitis
2. discoloration of urine (red/orange) and stools
VI Nursing Implications
A. Obtain a thorough medical history and assessment
B. perform liver function studies in pts who are to receive isoniazid or rifampin (esp in elderly pts or those who use alcohol daily)
C. Discontinue meds when liver enzymes rise to 4x higher than baseline.
SGOT = liver test. Watch tylenol consumption (or anything liver altering)
D. Assess for contraindications to the various agents, conditions for cautious use, and potential drug interactions
E. Patient education is critical
1. therapy may last up to 24 months
2. take meds exactly as ordered, at the same time everyday
3. emphasize the importance of strict compliance to regimen for improvement of condition or cure
4. remind pts that they are contagious during the initial period of their illness. Instruct in proper hygiene and prevention of the spread of infected droplets
5. emphasize to pts to take care of themselves, including adequate nutrition and rest
F. pts should not consume alcohol while on these meds or take other meds including OTC, unless they check with their physician
G. diabetic pts taking INH should monitor blood glucose levels b/c hyperglycemia may occur
H. INH and rifampin cause oral contraceptives to become ineffective; another form of birth control will be needed
I. Pts who are taking rifampin should be told that their urine, stool, salive, sputum, sweat, or tears may become reddish/orange; even contact lenses may be stained.
J. pyridoxine MUST be given with INH therapy to combat neuroligic side effects
K. Oral preparations may be given with meals to reduce GI upset, even though recommendations are to take them 1 hour before or 2 hours after meals.
L. Monitor for side effects
1. instruct pts on the side effects that should be reported to the physician immediately
2. these include fatigue, nausea, vomiting, numbness and tingling of the extremities, fever, loss of appetite, depression, jaundice
M. Monitor for therapeutic effects
1. decrease in symptoms of TB, such as cough and fever
2. lab studies (c&S tests) and CXR should confirm clinical findings
3. watch for lack of clinical response to therapy, indicating possible drug resistance
Antitubercular agents treat all forms of Mycobacterium
Chapter 40
I Tuberculosis
A. Caused by Mycobacterium tuberculosis
1. aerobic bacillus
2. passed from infected:
a. humans
b. cows (bovine)
c. birds (avian)
B. Common infection sites
1. lung (primary)
2. brain
3. bone
4. liver
5. kidney
C. infections
1. tubercle bacilli are conveyed by droplets
2. droplets are expelled by coughing or sneezing, then gain entry into the body by inhalation.
3. tubercle bacilli then spread to other body organs via blood and lymphatic systems
4. tubercle bacilli may become dormant, or walled off by calcified or fibrous tissue
II Antitubercular Agents *used in combination
A. First line
1. isoniazid (most frequently used)
2. ethambutol
3. pyrazinamide (PZA)
4. rafampin
5. streptomycin
B. second line agents (b/c of resistance)
1. capreomycin
2. cycloserine
3. ethionamide
4. kanamycin
5. para-aminosalicyclic acid (PAS)
III Mechanism of action (3 groups)
A. Protein wall synthesis inhibitors
1. streptomycin
2. kanamycin
3. capreomycin
4. rifampin
5. rifabutin
B. Cell wall synthesis inhibitors
1. cycloserine
2. ethionamide
3. isoniazid
a. drug of choice for TB
b. restistant strains of Mycobacterium emerging
c. metabolized in the liver through acetylation – watch for “slow acetylators”
d. used alone or in combination with other agents
e. indications
i. used for the prophylaxis or treatment of TB (for 6 months)
C. Other mechanisms of action
IV Antitubucular therapy
A. Effectiveness depends on:
1. type of infection
2. adequate dosing
3. sufficient duration of treatment
4. drug compliance
5. selection of an effective drug combination
6. resistance and compliance are a big problem
B. Problems
1. drug-resistant organisms
a. multidrug-resistant TB (MDR-TB)
2. drug toxicity
3. patient noncompliance
V Side Effects
A. INH (Isoniazid)
1. peripheral neuritis (inflammation of nerve endings)
2. hepatotoxicity
B. Ethambutol
1. retrobulbar neuritis
2. blindness
C. Rifampin
1. hepatitis
2. discoloration of urine (red/orange) and stools
VI Nursing Implications
A. Obtain a thorough medical history and assessment
B. perform liver function studies in pts who are to receive isoniazid or rifampin (esp in elderly pts or those who use alcohol daily)
C. Discontinue meds when liver enzymes rise to 4x higher than baseline.
SGOT = liver test. Watch tylenol consumption (or anything liver altering)
D. Assess for contraindications to the various agents, conditions for cautious use, and potential drug interactions
E. Patient education is critical
1. therapy may last up to 24 months
2. take meds exactly as ordered, at the same time everyday
3. emphasize the importance of strict compliance to regimen for improvement of condition or cure
4. remind pts that they are contagious during the initial period of their illness. Instruct in proper hygiene and prevention of the spread of infected droplets
5. emphasize to pts to take care of themselves, including adequate nutrition and rest
F. pts should not consume alcohol while on these meds or take other meds including OTC, unless they check with their physician
G. diabetic pts taking INH should monitor blood glucose levels b/c hyperglycemia may occur
H. INH and rifampin cause oral contraceptives to become ineffective; another form of birth control will be needed
I. Pts who are taking rifampin should be told that their urine, stool, salive, sputum, sweat, or tears may become reddish/orange; even contact lenses may be stained.
J. pyridoxine MUST be given with INH therapy to combat neuroligic side effects
K. Oral preparations may be given with meals to reduce GI upset, even though recommendations are to take them 1 hour before or 2 hours after meals.
L. Monitor for side effects
1. instruct pts on the side effects that should be reported to the physician immediately
2. these include fatigue, nausea, vomiting, numbness and tingling of the extremities, fever, loss of appetite, depression, jaundice
M. Monitor for therapeutic effects
1. decrease in symptoms of TB, such as cough and fever
2. lab studies (c&S tests) and CXR should confirm clinical findings
3. watch for lack of clinical response to therapy, indicating possible drug resistance
Antitubercular agents treat all forms of Mycobacterium
Antifungal
Antifungal Drugs
Chapter 41
Mechanism of action
Drug effects
Indications
I Fungal Infections
A. Fungi: very large and diverse group of microorganisms that include all yeasts and molds.
1. yeasts:
a. single celled fungi
b. reproduce by budding.
c. also used for baking and alcoholic beverages
2. molds:
a. multicellular.
b. Characterized by long, branching filaments called hyphae.
B. fungal infections aka mycoses (mycotic infections)
1. cutaneous
2. subcutaneous
3. superficial
4. systemic
a. usually occur in an immunocomprimised host
b. can be life threatening
5. diseases
a. Candida albicans
i. due to antibiotic therapy, antineoplastics, or immunosuppressants (corticosteroids)
ii. may result in overgrowth and systemic infections
b. in the mouth
i. oral candidiasis or thrush
ii. newborn infants and immunocompromised patients
iii. contagious
c. vaginal candidiasis
i. “yeast infection”
ii. pregnancy, diabetes mellitus, oral contraceptives, antibiotics
C. some fungi are part of the normal flora of the skin, mouth, intestines, and vagina.
II Antifungal agents:
A. drugs used to treat infections caused by fungi
B. systemic work in the blood stream
C. topical work on the skin
D. broken down into major groups based on their mechanisms of action
E. Agents
1. Polyenes
a. amphotericin B
b. nystatin
2. flucytosine
3. imidazoles
a. ketoconazole
b. muconazole
c. clotrimazole
d. fluconazole
4. griseofulvin
5. allylmine
a. terbinafine
III Mechanism of Action
A. polyenes (amphotericin B and nystatin)
1. bind to sterols in cell membrane lining
2. result: fungal death
3. do not bind to human cell membranes or kill human cells
B. flucytosine
1. aka 5-fluorocytosine (antimetabolite)
2. taken up by fungal cells and interferes with DNA synthesis
3. result: fungal cell death
C. imidazoles (...azoles)
1. inhibit an enzyme, resulting in cell membrane leaking
2. lead to altered cell membrane
3. result: fungal death
D. Griseofulvin
1. disrupts cell division
2. result: inhibited fungal mitosis (reproduction)
IV Indications (systemic and topical fungal infections)
A. Choice of agent depends on type and location of infection
B. Agent of choice for the treatment of many severe systemic fungal infections is amphotericin B
V Side Effects
A. Amphotericin B “shake and bake”
1. fever
2. headache
3. chills
4. malaise
5. hypotension
6. muscle and joint pain
7. lowered potassium and magnesium levels
8. dysrhythmias
9. nausea
10. anorexia
11. main concern is renal toxicity (b/c renally eliminated)
12. neurotoxicity: seizures and paresthesias
B. fluconazole
1. nausea, vomiting, diarrhea, stomach pain
2. increased liver function studies
C. flucytosine
1. n/v, anorexia, headache, dizziness, others
D. griseofulvin
1. rash, urticaria, headache, n/v, anorexia, others
VI Nursing Implications
A. Before beginning therapy, assess for hypersensitivity, possible contraindications, and conditions that require cautious use.
B. Obtain baseline VS, CBC, liver function studies, and ECG
C. Assess for other medcations used (prescribed and OTC) in order to avoid drug interactions.
D. Follow manufacturer’s directions carefully for reconstitution and admin.
E. Monitor VS’s op patients receiving IV infusions every 15 – 30 minutes
F. During IV infusions, monitor I & O and urinalysis findings to identify adverse renal effects.
G. Amphotericin B
a. to reduce the severity of the infusion-related reactions, pretreatment with an antipyretic (acetaminophin), antihistamines, and antiemetics may be given.
b. A test dose of 1mg per 20ml 5% dextrose in water infused over 30 min should be given.
c. use iv infusion pumps and the most distal veins possible
H. Tissue extravasation of fluconazole at the iv site may lead to tissue necrosis. Monitor the iv site carefully.
I. Oral forms of griseofulvin should be given with meals to decrease GI upset.
J. Monitor carefully for side/adverse effects
K. Monitor for therapeutic effects
1. easing for the sympotoms of infection
2. improved energy levels
3. normal vital signs, including temp
Questions
Are fungal infections are difficult to treat. True
Know that oral candidiasis is contagious.
How would we prevent side effects? Tylenol, steroid, antihistamine.
Chapter 41
Mechanism of action
Drug effects
Indications
I Fungal Infections
A. Fungi: very large and diverse group of microorganisms that include all yeasts and molds.
1. yeasts:
a. single celled fungi
b. reproduce by budding.
c. also used for baking and alcoholic beverages
2. molds:
a. multicellular.
b. Characterized by long, branching filaments called hyphae.
B. fungal infections aka mycoses (mycotic infections)
1. cutaneous
2. subcutaneous
3. superficial
4. systemic
a. usually occur in an immunocomprimised host
b. can be life threatening
5. diseases
a. Candida albicans
i. due to antibiotic therapy, antineoplastics, or immunosuppressants (corticosteroids)
ii. may result in overgrowth and systemic infections
b. in the mouth
i. oral candidiasis or thrush
ii. newborn infants and immunocompromised patients
iii. contagious
c. vaginal candidiasis
i. “yeast infection”
ii. pregnancy, diabetes mellitus, oral contraceptives, antibiotics
C. some fungi are part of the normal flora of the skin, mouth, intestines, and vagina.
II Antifungal agents:
A. drugs used to treat infections caused by fungi
B. systemic work in the blood stream
C. topical work on the skin
D. broken down into major groups based on their mechanisms of action
E. Agents
1. Polyenes
a. amphotericin B
b. nystatin
2. flucytosine
3. imidazoles
a. ketoconazole
b. muconazole
c. clotrimazole
d. fluconazole
4. griseofulvin
5. allylmine
a. terbinafine
III Mechanism of Action
A. polyenes (amphotericin B and nystatin)
1. bind to sterols in cell membrane lining
2. result: fungal death
3. do not bind to human cell membranes or kill human cells
B. flucytosine
1. aka 5-fluorocytosine (antimetabolite)
2. taken up by fungal cells and interferes with DNA synthesis
3. result: fungal cell death
C. imidazoles (...azoles)
1. inhibit an enzyme, resulting in cell membrane leaking
2. lead to altered cell membrane
3. result: fungal death
D. Griseofulvin
1. disrupts cell division
2. result: inhibited fungal mitosis (reproduction)
IV Indications (systemic and topical fungal infections)
A. Choice of agent depends on type and location of infection
B. Agent of choice for the treatment of many severe systemic fungal infections is amphotericin B
V Side Effects
A. Amphotericin B “shake and bake”
1. fever
2. headache
3. chills
4. malaise
5. hypotension
6. muscle and joint pain
7. lowered potassium and magnesium levels
8. dysrhythmias
9. nausea
10. anorexia
11. main concern is renal toxicity (b/c renally eliminated)
12. neurotoxicity: seizures and paresthesias
B. fluconazole
1. nausea, vomiting, diarrhea, stomach pain
2. increased liver function studies
C. flucytosine
1. n/v, anorexia, headache, dizziness, others
D. griseofulvin
1. rash, urticaria, headache, n/v, anorexia, others
VI Nursing Implications
A. Before beginning therapy, assess for hypersensitivity, possible contraindications, and conditions that require cautious use.
B. Obtain baseline VS, CBC, liver function studies, and ECG
C. Assess for other medcations used (prescribed and OTC) in order to avoid drug interactions.
D. Follow manufacturer’s directions carefully for reconstitution and admin.
E. Monitor VS’s op patients receiving IV infusions every 15 – 30 minutes
F. During IV infusions, monitor I & O and urinalysis findings to identify adverse renal effects.
G. Amphotericin B
a. to reduce the severity of the infusion-related reactions, pretreatment with an antipyretic (acetaminophin), antihistamines, and antiemetics may be given.
b. A test dose of 1mg per 20ml 5% dextrose in water infused over 30 min should be given.
c. use iv infusion pumps and the most distal veins possible
H. Tissue extravasation of fluconazole at the iv site may lead to tissue necrosis. Monitor the iv site carefully.
I. Oral forms of griseofulvin should be given with meals to decrease GI upset.
J. Monitor carefully for side/adverse effects
K. Monitor for therapeutic effects
1. easing for the sympotoms of infection
2. improved energy levels
3. normal vital signs, including temp
Questions
Are fungal infections are difficult to treat. True
Know that oral candidiasis is contagious.
How would we prevent side effects? Tylenol, steroid, antihistamine.
Antibiotics
Antibiotics
Chapter 37
Antibiotics
I Definition:
A. medications used to treat bacterial infections
B. Ideally, before beginning antibiotic therapy, the suspected areas of infection should be cultured to identify the causative organism and potential antibiotic susceptibilities
II Classes
A. Sulfonamides
B. Penicillins
C. Cephalosporins
D. Tetracyclines
E. Macrolides
F. Aminoglycosides
G. Quinolones
III Antibiotic Therapy
A. Empiric therapy: treatment of an infection before specific culture information has been reported or obtained
B. Prophylactic therapy: treatment with antibiotics to prevent an infection, as in intraabdominal surgery.
C. Therapeutic response:
Decrease in specific signs and symptoms of infection are noted (fever, elevated WBC, redness, inflammation, drainage, pain)
1. Streamline therapy: after results from C&S come back, change to the appropriate antibiotic. (narrow down) Broad spectrum causes resistance.
D. Subtherapeutic response:
Signs and symptoms of infection do not improve.
1. Superinfection: occurs when antibiotics reduce or completely eliminate the normal bacterial flora
2. antibiotic resistance:
3. host factors: age, allergy history, kidney and liver function, pregnancy, genetic characteristics, site of infection, host defenses
4. genetic host factors
a. G6PD deficiency
b. slow acetylator metabolic status
5. allergic reactions: especially to pcn (any “illins”) and sulfa drugs
IV Mechanism of Action
A. Interference with cell wall synthesis
B. Interference with protein synthesis
C. Interference with DNA replication
D. Acting as a metabolite to disrupt critical metabolic reactions inside the bacterial cell
E. Actions of Antibiotics
1. bactericidal: kill bacteria
2. bacteriostatic: inhibit growth of susceptible bacteria, rather than killing them immediately; will eventually lead to bacterial death
Sulfonamides
I Definition: one of the first groups of antibiotics.
II Drugs:
A. sulfadiazine
B. sulfamethoxazole: primary one used today in combination w/another antib.
C. sulfisoxazole
III Mechanism of Action
A. Bacteriostatic action
B. prevent synthesis of folic acid required for synthesis of purines and nucleic acid
C. Do not affect human cells or certain bacteria, they can use preformed folic acid
IV Indications
A. Treatment of UTI’s caused by susceptible strains of:
1. Enterobacter
2. Escherichia coli
3. Klebsiella
4. Proteus mirabilis
5. Proteus vulgaris
6. Staphylococcus aureus
B. Nocardiosis
C. Pneumocystis carinii pneumonia (PCP) co-trimoxazole This is a protozoa, not a bacteria. It is best treated by sulfonamides. Bactrim. Use high doses.
D. Upper respiratory tract infections
E. other uses
V Sulfanomides: Combination products
A. trimethoprim/sulfamethoxazole (Bactrm, Septra)
1. used to treat UTI’s, PCP, otitis media, others.
2. drink alot of water.
3. Don’t really use sulfa products alone anymore; we combine them so they work better.
VI Side effects:
Stevens-Johnson syndrome, epidermal necrolysis
Beta-Lactam Antibiotics
Penicillins
I Types
A. Natural penicillins
1. penicillin G
2. penicillin V potassium
B. Penicillinase-resistant penicillins (after natural became resistant we used these, didn’t last long)
1. cloxacillin
2. dicloxacillin
4. nafcillin
5. oxacillin
C. aminopenicillins (became resistant)
1. amoxicillin
2. ampicillin
3. bacampicillin
D. extended-spectrum penicillins
1. piperacillin
2. ticarcillin
3. carbenicillin
E. Can take monobactam if allergic to pcn, not cephalosporin or carbapenems.
II Facts
A. first introduced in the 1940’s, discovered by Fleming
B. bacteriacidal: inhibit cell wall synthesis
C. kill a wide variety of bacteria
D. also called beta lactams
E. bacteria produce enzymes called beta-lactamases which are capable of destroying penicillins. As a result, the medication is not effective. This is a method of resistance.
F. Chemicals have been developed to inhibit these enzymes. They bind with beta-lactamase and prevent the enzyme from breaking down the pcn.
1. clavulanic acid ( + ticarcillin = Timentin)
2. tazobactam (+ piperacillin = Zosyn)
3. sulbactam (+ampicillin = Unasyn)
4. clavulanic acid (+amoxicillin = Augmentin)
III Mechanism of Action
A. enter the bacteria via the cell wall
B. inside the cell they bind to penicillin binding protein
C. once bound, normal cell wall synthesis is disrupted
D. Result: bacteria cells die from lysis
IV Indications
A. prevention and treatment of infections caused by susceptible bacteria, such as:
1. gram + bacteria
2. Streptococcus, Enterococcus, Staphylococcus
V Adverse Effects
A. allergic reactions occur in 0.7% to 8% of cases
1. urticaria
2. pruritus
3. angioedema
B. 10% of allergic reactions are life threatening
1. 10% of these are fatal (All can be life threatening, all can be fatal)
VI Side effects
A. common: n/v, diarr, abd pain...others are less common
Beta-Lactam Antibiotics
Cephalospporins
I Types
A. 1st generation (good gram + coverage. Poor gram – coverage.)
1. cephalexin (Keflex) PO
2. cefazolin (Ancef and Kefzol) IV only
3. used for surgical prophylaxis, URI’s, otitis media
B. 2nd generation
1. good gram + coverage, better gram – than 1st generation
2. cefoxitin (Mefoxin) IV and IM
a. used prophylactically for abd or colorectal surgeries
b. kills anaerobes
3. cefuroxime (Kefurox and Ceftin) PO
a. surgical prophylaxis
b. does not kill anaerobes
C. 3rd generation
1. most potent group against gram negative, less active against gram +
2. ceftriaxone (Rocephin)
a. IV and IM
b. long ½ life
c. once a day dosing
d. easily passes meninges and diffused into CDF to treat CNS infections. Great for meningitis and shingles
e. NOT RENALLY ELIMINATED billiary/liver so can cause diarrhea.
f. covers all/most gram – and strepto pneumon, gonorrhea. (does not cover pseudomonas)
3. ceftazidime (ceptaz, fortaz, taxidime, tazicef)
a. IV and IM
b. excellent gram – coverage
c. used for difficult to treat organisms such as Pseudomonas
4. cefixime (Suprax) ONLY ORAL 3RD GENERATION AGENT
a. best of available oral cephalosporins against gram –
b. tablet and suspension
D. 4th generation
1. cefepime (Maxipime)
2. newest
3. broader spectrum esp against gram +
II Facts
A. semisynthetic derivatives from a fungus
B. structurally and pharmacologically related to pcn
C. Bacteriacidal
D. broad spectrum
E. divided into groups according to their antimicrobial activity
III Side effects
A. similar to pcn
Beta-Lactam Antibiotics
Carbapenems
I Facts
A. very broad spectrum antibacterial action
B. reserved for complicated body cavity and connective tissue infections
C. may cause drug induced seizure activity (imipenem-cilastatin...Primaxin)
D. used for treatment of bone, joint, skin, and soft tissue infections; many other uses
E. if allergic to pcn, allergic to this also
Beta-Lactam Antibiotics
Monobactams
I Facts
A. aztreonam (Azactam)
B. synthetic
C. primarily active against aerobic gram – bacteria (E. coli, Klebsiella, Pseudomonas)
D. If you are allergic to pcn you CAN take this
Macrolides
I Types
A. erythromycin (Emycin, EES)
B. azithromycin (Zithromax)
C. clarithromycin (Biaxin)
II Mechanism of Action
A. prevent protein synthesis within bacterial cells
B. bacteria will eventually die
C. bacteriastatic
D. all liver metabolized
III Indications (treat atypical organisms)
A. strep infections
B. mild to moderate URI
C. haemophilus influenzae
D. spirochetal infections
1. syphillis
2. lyme disease
E. gonorrhea, chlamydia, mycoplasma
IV Side effects
A. GI effects primarily with erythromycin
B. newer agents fewer side effects, better action
1. azithromycin
2. clarithromycin: bad metallid taste in mouth
Tetracyclines
I types
A. tetracyline: used for acne. Discolors teeth, crosses placenta & breastmilk
B. demeclocycline is also used to treat SIADH And pleural and pericardial effusions (symptoms of inappropriate ADH)
II Facts
A. natural and synthetic
B. obtained from cultures of streptomyces
C. bacteriostatic
D. inhibit protein synthesis
E. stop many essential function of the bacteria
F. Dairy products, antacids, and iron salts reduce absorption of tetras Has a strong affinity for calcium.
1. discoloration of permanent teeth and tooth enamel in fetuses and children
2. may retard fetal skeletal develop if taken during pregnancy
III Indications
A. wide spectrum
1. gram -, gram +, protozoa, mycoplasma, rickettsia, chlamydia, syphilis, lyme disease
IV Side effects
A. discoloration of permanent teeth and tooth enamel in fetuses and children
B. may retard fetal skeletal develop if taken during pregnancy
C. Alteration in intestinal flora may result in:
1. superinfection (overgrowth)
2. diarrhea
3. pseudomembranous colitis/bloody diarrhea
D. may also cause:
1. vaginal moniliasis
2. gastric upset
3. enterocolitis
4. maculopapular rash
Aminoglycosides
I Types (systemic)
A. gentamicin (Garamycin)
B. tobramycin
C. amikacin (Amikin)
II Facts
A. natural and semisynthetic
B. produced from streptomyces
C. poor oral absorption NO PO FORMS
D. very potent antibiotics with serious toxicities
E. Bacteriacidal
F. kills mostly gram –
G. Narrow therapeutic window. We must pull levels on this. Serious toxicities.
H. TOXIC TO KIDNEYS AND EARS
III Indications
A. kill gram -. Pseudomonas, e. coli, proteus, klebsiella, serratia
B. often used in combination with others for synergistic effect
C. narrow therapeutic window medications
D. All poorly absorbed through GI, the exception is neomycin.
1. given orally to decontaminate the gi tract before surgery
2. also used as an enema for this purpose
IV Side effects
A. cause serious toxicities
1. nephrotoxicity
2. ototoxicity: auditory impairment and vestibular 8th cranial nerve
B. must monitor drug levels to prevent toxicities
C. headache, paresthesia, dizziness, vertigo, skin rash, fever, superinfection
Quinolones
I Types
A. ciprofloxacin (cipro)
B. levofloxacin (levaquin)
II Facts
A. excellent oral absorption, as good as an IV
B. absorption reduced by antacids
C. first oral antibiotics effective against gram- bacteria (some +)
D. bactericidal
III Indications
A. Anthrax among others
IV Side effects
A. headache, dizziness, depression
B. n/v/d/constipation/
C. rash, photosensitvity
D. fever chills, blurred vision, tinnitus
Other
I Vancomycin (stands alone)
A. treatment of choice for MRSA and other gram +
B. monitor blood levels
C. ototoxicity and nephrotoxicity
D. should be infused over 90 minutes
E. Redman’s syndrome
Nursing implications
It is essential to obtain cultures from appropriate sites before beginning therapy.
Take exactly as prescribed and for the length of time prescribed.
Assess for superinfection.
Check the name of med carefully because of look/sound alikes
Take w/ 6-8 oz water
Most common side effects: n/v/d
Sulfonamides:
Take w/2000 ml fluid/day
Photosensitivity
Reduce contraceptives
Take w/food or milk to reduce upset
Penicillins
Allergic rxn for 30 min
Decreased w/caffeine, citrus, cola, tomato juice
Cephalosporins
Give w/food
No alcohol
Tetracyclines
Avoid dairy b/c of chelation
Photosensitivity
Aminoglycides
Nephrotoxicity....peak and trough levels
Ototoxicity...dizziness, tinnitus, hearing loss
Test Questions:
Penicillins can cause seizures if dosed too high. True.
(renally eliminated, if bad renal function...retain more drug.)
What was added to penicillins to prevent beta-lactamases from working?
Clavulanic acid, tazobactam, sulbactam.
Bacteriastatic
Macrolides
Tetracycline
sulfonamides
Bactericidal
Aminoglycosides
Quinolones
Pencillin
Cephalosporins
Carbapenems
Monobactams
vancomycin
Chapter 37
Antibiotics
I Definition:
A. medications used to treat bacterial infections
B. Ideally, before beginning antibiotic therapy, the suspected areas of infection should be cultured to identify the causative organism and potential antibiotic susceptibilities
II Classes
A. Sulfonamides
B. Penicillins
C. Cephalosporins
D. Tetracyclines
E. Macrolides
F. Aminoglycosides
G. Quinolones
III Antibiotic Therapy
A. Empiric therapy: treatment of an infection before specific culture information has been reported or obtained
B. Prophylactic therapy: treatment with antibiotics to prevent an infection, as in intraabdominal surgery.
C. Therapeutic response:
Decrease in specific signs and symptoms of infection are noted (fever, elevated WBC, redness, inflammation, drainage, pain)
1. Streamline therapy: after results from C&S come back, change to the appropriate antibiotic. (narrow down) Broad spectrum causes resistance.
D. Subtherapeutic response:
Signs and symptoms of infection do not improve.
1. Superinfection: occurs when antibiotics reduce or completely eliminate the normal bacterial flora
2. antibiotic resistance:
3. host factors: age, allergy history, kidney and liver function, pregnancy, genetic characteristics, site of infection, host defenses
4. genetic host factors
a. G6PD deficiency
b. slow acetylator metabolic status
5. allergic reactions: especially to pcn (any “illins”) and sulfa drugs
IV Mechanism of Action
A. Interference with cell wall synthesis
B. Interference with protein synthesis
C. Interference with DNA replication
D. Acting as a metabolite to disrupt critical metabolic reactions inside the bacterial cell
E. Actions of Antibiotics
1. bactericidal: kill bacteria
2. bacteriostatic: inhibit growth of susceptible bacteria, rather than killing them immediately; will eventually lead to bacterial death
Sulfonamides
I Definition: one of the first groups of antibiotics.
II Drugs:
A. sulfadiazine
B. sulfamethoxazole: primary one used today in combination w/another antib.
C. sulfisoxazole
III Mechanism of Action
A. Bacteriostatic action
B. prevent synthesis of folic acid required for synthesis of purines and nucleic acid
C. Do not affect human cells or certain bacteria, they can use preformed folic acid
IV Indications
A. Treatment of UTI’s caused by susceptible strains of:
1. Enterobacter
2. Escherichia coli
3. Klebsiella
4. Proteus mirabilis
5. Proteus vulgaris
6. Staphylococcus aureus
B. Nocardiosis
C. Pneumocystis carinii pneumonia (PCP) co-trimoxazole This is a protozoa, not a bacteria. It is best treated by sulfonamides. Bactrim. Use high doses.
D. Upper respiratory tract infections
E. other uses
V Sulfanomides: Combination products
A. trimethoprim/sulfamethoxazole (Bactrm, Septra)
1. used to treat UTI’s, PCP, otitis media, others.
2. drink alot of water.
3. Don’t really use sulfa products alone anymore; we combine them so they work better.
VI Side effects:
Stevens-Johnson syndrome, epidermal necrolysis
Beta-Lactam Antibiotics
Penicillins
I Types
A. Natural penicillins
1. penicillin G
2. penicillin V potassium
B. Penicillinase-resistant penicillins (after natural became resistant we used these, didn’t last long)
1. cloxacillin
2. dicloxacillin
4. nafcillin
5. oxacillin
C. aminopenicillins (became resistant)
1. amoxicillin
2. ampicillin
3. bacampicillin
D. extended-spectrum penicillins
1. piperacillin
2. ticarcillin
3. carbenicillin
E. Can take monobactam if allergic to pcn, not cephalosporin or carbapenems.
II Facts
A. first introduced in the 1940’s, discovered by Fleming
B. bacteriacidal: inhibit cell wall synthesis
C. kill a wide variety of bacteria
D. also called beta lactams
E. bacteria produce enzymes called beta-lactamases which are capable of destroying penicillins. As a result, the medication is not effective. This is a method of resistance.
F. Chemicals have been developed to inhibit these enzymes. They bind with beta-lactamase and prevent the enzyme from breaking down the pcn.
1. clavulanic acid ( + ticarcillin = Timentin)
2. tazobactam (+ piperacillin = Zosyn)
3. sulbactam (+ampicillin = Unasyn)
4. clavulanic acid (+amoxicillin = Augmentin)
III Mechanism of Action
A. enter the bacteria via the cell wall
B. inside the cell they bind to penicillin binding protein
C. once bound, normal cell wall synthesis is disrupted
D. Result: bacteria cells die from lysis
IV Indications
A. prevention and treatment of infections caused by susceptible bacteria, such as:
1. gram + bacteria
2. Streptococcus, Enterococcus, Staphylococcus
V Adverse Effects
A. allergic reactions occur in 0.7% to 8% of cases
1. urticaria
2. pruritus
3. angioedema
B. 10% of allergic reactions are life threatening
1. 10% of these are fatal (All can be life threatening, all can be fatal)
VI Side effects
A. common: n/v, diarr, abd pain...others are less common
Beta-Lactam Antibiotics
Cephalospporins
I Types
A. 1st generation (good gram + coverage. Poor gram – coverage.)
1. cephalexin (Keflex) PO
2. cefazolin (Ancef and Kefzol) IV only
3. used for surgical prophylaxis, URI’s, otitis media
B. 2nd generation
1. good gram + coverage, better gram – than 1st generation
2. cefoxitin (Mefoxin) IV and IM
a. used prophylactically for abd or colorectal surgeries
b. kills anaerobes
3. cefuroxime (Kefurox and Ceftin) PO
a. surgical prophylaxis
b. does not kill anaerobes
C. 3rd generation
1. most potent group against gram negative, less active against gram +
2. ceftriaxone (Rocephin)
a. IV and IM
b. long ½ life
c. once a day dosing
d. easily passes meninges and diffused into CDF to treat CNS infections. Great for meningitis and shingles
e. NOT RENALLY ELIMINATED billiary/liver so can cause diarrhea.
f. covers all/most gram – and strepto pneumon, gonorrhea. (does not cover pseudomonas)
3. ceftazidime (ceptaz, fortaz, taxidime, tazicef)
a. IV and IM
b. excellent gram – coverage
c. used for difficult to treat organisms such as Pseudomonas
4. cefixime (Suprax) ONLY ORAL 3RD GENERATION AGENT
a. best of available oral cephalosporins against gram –
b. tablet and suspension
D. 4th generation
1. cefepime (Maxipime)
2. newest
3. broader spectrum esp against gram +
II Facts
A. semisynthetic derivatives from a fungus
B. structurally and pharmacologically related to pcn
C. Bacteriacidal
D. broad spectrum
E. divided into groups according to their antimicrobial activity
III Side effects
A. similar to pcn
Beta-Lactam Antibiotics
Carbapenems
I Facts
A. very broad spectrum antibacterial action
B. reserved for complicated body cavity and connective tissue infections
C. may cause drug induced seizure activity (imipenem-cilastatin...Primaxin)
D. used for treatment of bone, joint, skin, and soft tissue infections; many other uses
E. if allergic to pcn, allergic to this also
Beta-Lactam Antibiotics
Monobactams
I Facts
A. aztreonam (Azactam)
B. synthetic
C. primarily active against aerobic gram – bacteria (E. coli, Klebsiella, Pseudomonas)
D. If you are allergic to pcn you CAN take this
Macrolides
I Types
A. erythromycin (Emycin, EES)
B. azithromycin (Zithromax)
C. clarithromycin (Biaxin)
II Mechanism of Action
A. prevent protein synthesis within bacterial cells
B. bacteria will eventually die
C. bacteriastatic
D. all liver metabolized
III Indications (treat atypical organisms)
A. strep infections
B. mild to moderate URI
C. haemophilus influenzae
D. spirochetal infections
1. syphillis
2. lyme disease
E. gonorrhea, chlamydia, mycoplasma
IV Side effects
A. GI effects primarily with erythromycin
B. newer agents fewer side effects, better action
1. azithromycin
2. clarithromycin: bad metallid taste in mouth
Tetracyclines
I types
A. tetracyline: used for acne. Discolors teeth, crosses placenta & breastmilk
B. demeclocycline is also used to treat SIADH And pleural and pericardial effusions (symptoms of inappropriate ADH)
II Facts
A. natural and synthetic
B. obtained from cultures of streptomyces
C. bacteriostatic
D. inhibit protein synthesis
E. stop many essential function of the bacteria
F. Dairy products, antacids, and iron salts reduce absorption of tetras Has a strong affinity for calcium.
1. discoloration of permanent teeth and tooth enamel in fetuses and children
2. may retard fetal skeletal develop if taken during pregnancy
III Indications
A. wide spectrum
1. gram -, gram +, protozoa, mycoplasma, rickettsia, chlamydia, syphilis, lyme disease
IV Side effects
A. discoloration of permanent teeth and tooth enamel in fetuses and children
B. may retard fetal skeletal develop if taken during pregnancy
C. Alteration in intestinal flora may result in:
1. superinfection (overgrowth)
2. diarrhea
3. pseudomembranous colitis/bloody diarrhea
D. may also cause:
1. vaginal moniliasis
2. gastric upset
3. enterocolitis
4. maculopapular rash
Aminoglycosides
I Types (systemic)
A. gentamicin (Garamycin)
B. tobramycin
C. amikacin (Amikin)
II Facts
A. natural and semisynthetic
B. produced from streptomyces
C. poor oral absorption NO PO FORMS
D. very potent antibiotics with serious toxicities
E. Bacteriacidal
F. kills mostly gram –
G. Narrow therapeutic window. We must pull levels on this. Serious toxicities.
H. TOXIC TO KIDNEYS AND EARS
III Indications
A. kill gram -. Pseudomonas, e. coli, proteus, klebsiella, serratia
B. often used in combination with others for synergistic effect
C. narrow therapeutic window medications
D. All poorly absorbed through GI, the exception is neomycin.
1. given orally to decontaminate the gi tract before surgery
2. also used as an enema for this purpose
IV Side effects
A. cause serious toxicities
1. nephrotoxicity
2. ototoxicity: auditory impairment and vestibular 8th cranial nerve
B. must monitor drug levels to prevent toxicities
C. headache, paresthesia, dizziness, vertigo, skin rash, fever, superinfection
Quinolones
I Types
A. ciprofloxacin (cipro)
B. levofloxacin (levaquin)
II Facts
A. excellent oral absorption, as good as an IV
B. absorption reduced by antacids
C. first oral antibiotics effective against gram- bacteria (some +)
D. bactericidal
III Indications
A. Anthrax among others
IV Side effects
A. headache, dizziness, depression
B. n/v/d/constipation/
C. rash, photosensitvity
D. fever chills, blurred vision, tinnitus
Other
I Vancomycin (stands alone)
A. treatment of choice for MRSA and other gram +
B. monitor blood levels
C. ototoxicity and nephrotoxicity
D. should be infused over 90 minutes
E. Redman’s syndrome
Nursing implications
It is essential to obtain cultures from appropriate sites before beginning therapy.
Take exactly as prescribed and for the length of time prescribed.
Assess for superinfection.
Check the name of med carefully because of look/sound alikes
Take w/ 6-8 oz water
Most common side effects: n/v/d
Sulfonamides:
Take w/2000 ml fluid/day
Photosensitivity
Reduce contraceptives
Take w/food or milk to reduce upset
Penicillins
Allergic rxn for 30 min
Decreased w/caffeine, citrus, cola, tomato juice
Cephalosporins
Give w/food
No alcohol
Tetracyclines
Avoid dairy b/c of chelation
Photosensitivity
Aminoglycides
Nephrotoxicity....peak and trough levels
Ototoxicity...dizziness, tinnitus, hearing loss
Test Questions:
Penicillins can cause seizures if dosed too high. True.
(renally eliminated, if bad renal function...retain more drug.)
What was added to penicillins to prevent beta-lactamases from working?
Clavulanic acid, tazobactam, sulbactam.
Bacteriastatic
Macrolides
Tetracycline
sulfonamides
Bactericidal
Aminoglycosides
Quinolones
Pencillin
Cephalosporins
Carbapenems
Monobactams
vancomycin
Nitrates Nitrites
Nitrates/Nitrites
I Available forms:
A. sublingual
B. buccal
C. chewable tables
D. oral capsules/tablets
E. iv
F. ointments
G. transdermal patches
H. translingual sprays (do not shake)
II Mechanism of action
A. cause vasodilation due to relaxation of smooth muscles
B. potent dilating effect on coronary arteries
C. used for prevention and treatment of angina
D. vasodilation results in reduced myocardial O2 demand
E. nitrates cause dilation of both large and small coronary vessels
F. result: O2 to ischemic myocardial tissue
G. nitrates alleviate coronary artery spasms
III Types
A. Nitroglycerin
1. prototypical nitrate
2. large first pass effect w/oral forms
3. Indications
a. used for symptomatic tx of ischemic heart conditions (angina)
b. IV form used for bp control in perioperative hpn, tx of hf, ischemic pain, pulmonary edema assoc w/ acute MI, and HPN emergencies
4. Dosages
a. Nitroglycerin SL (usuallly 0.4 mg) Place one under tongue every 5 minutes x 3 for chest pain. If still pain after 5 min call 911. Should be kept in original container. Once opened replace every 6 months. Side effect of headache should NOT deter use.
5. Nursing implications:
a. take prn nitrates at the first hint of anginal pain
b. the pt taking SL NTG should be lying down to prevent or decrease dizziness and fainting that may occur due to hypotension
c. make sure pts have a nitrate free period of 8-12 hours. Put on patch in am, take off @ night.
d. instruct pts in proper technique/guidelines for SL NTG
e. instruct pts in proper application of ointment and transdermal forms
f. “ “ site rotation & removal of old med daily
g. never chew or swallow the SL form
h. keep a fresh supply of NTG on hand
i. Burning sensation felt w/ SL = drug still potent
j. potency lost after bottle opened for 3 months
k. store in airtight, dark glass bottle w/a metal cap and not cotton filler to preserve potency
l. IV forms of NTG must be contained in glass & given w/infusion pumps
m. discard parenteral soln that is blue, green, or dark red
n. follow specific manuf instructions for Iv admin; use special IV tubing provided or non PVC tubing
B. Nitrates
1. types
a. Isosorbide dinitrate
i. Isordil
ii. Sorbitrate
iii. Dilatrate SR
b. Isosorbide mononitrate
i. Imdur
ii. Monoket
iii. ISMO
2. indications
a. acute relief of angina
b. prophylaxis in situations that may provoke angina
c. long term prophylaxis of angina
3. Side effects
a. headache: usually diminish in intensity and frequency after continued use
b. tachycardia
c. postural hypotension
d. tolerance may develop and need higher doses to be effective
I Available forms:
A. sublingual
B. buccal
C. chewable tables
D. oral capsules/tablets
E. iv
F. ointments
G. transdermal patches
H. translingual sprays (do not shake)
II Mechanism of action
A. cause vasodilation due to relaxation of smooth muscles
B. potent dilating effect on coronary arteries
C. used for prevention and treatment of angina
D. vasodilation results in reduced myocardial O2 demand
E. nitrates cause dilation of both large and small coronary vessels
F. result: O2 to ischemic myocardial tissue
G. nitrates alleviate coronary artery spasms
III Types
A. Nitroglycerin
1. prototypical nitrate
2. large first pass effect w/oral forms
3. Indications
a. used for symptomatic tx of ischemic heart conditions (angina)
b. IV form used for bp control in perioperative hpn, tx of hf, ischemic pain, pulmonary edema assoc w/ acute MI, and HPN emergencies
4. Dosages
a. Nitroglycerin SL (usuallly 0.4 mg) Place one under tongue every 5 minutes x 3 for chest pain. If still pain after 5 min call 911. Should be kept in original container. Once opened replace every 6 months. Side effect of headache should NOT deter use.
5. Nursing implications:
a. take prn nitrates at the first hint of anginal pain
b. the pt taking SL NTG should be lying down to prevent or decrease dizziness and fainting that may occur due to hypotension
c. make sure pts have a nitrate free period of 8-12 hours. Put on patch in am, take off @ night.
d. instruct pts in proper technique/guidelines for SL NTG
e. instruct pts in proper application of ointment and transdermal forms
f. “ “ site rotation & removal of old med daily
g. never chew or swallow the SL form
h. keep a fresh supply of NTG on hand
i. Burning sensation felt w/ SL = drug still potent
j. potency lost after bottle opened for 3 months
k. store in airtight, dark glass bottle w/a metal cap and not cotton filler to preserve potency
l. IV forms of NTG must be contained in glass & given w/infusion pumps
m. discard parenteral soln that is blue, green, or dark red
n. follow specific manuf instructions for Iv admin; use special IV tubing provided or non PVC tubing
B. Nitrates
1. types
a. Isosorbide dinitrate
i. Isordil
ii. Sorbitrate
iii. Dilatrate SR
b. Isosorbide mononitrate
i. Imdur
ii. Monoket
iii. ISMO
2. indications
a. acute relief of angina
b. prophylaxis in situations that may provoke angina
c. long term prophylaxis of angina
3. Side effects
a. headache: usually diminish in intensity and frequency after continued use
b. tachycardia
c. postural hypotension
d. tolerance may develop and need higher doses to be effective
Calcium Channel Blockers
Calcium Channel Blockers
I Types
A. verapamil (calan)
B. diltiazem (Cardizem)
C. nifedipine (Procardia)
II Mechanism of Action
A. Cause peripheral arterial vasodilation
B. reduce myocardial contractility (negative inotropic action)
C. result: decreased myocardial O2 demand
III Indications
A. First line agents for tx of angina, HPN and supraventricular tachy arryth
B. short term mgmt of atrial fibrillation and flutter
IV Side effects
A. very acceptable side effects and safety profile
B. may cause:
1. hypotension
2. palpitations
3. tachycardia or bradycardia
4. constipation
5. nausea
6. dyspnea
V Nursing implications
A. blood levels should be monitored to ensure they are therapeutic
B. oral CCBs should be taken before meals and as ordered
C. pts should be encouraged to limit caffeine intake
D. before administering, perform a complete health history to determine presence of conditions that may be contraindications for use or call for cautious use
E. obtain baseline VS, including respiratory patterns and rate
F. access for drug interactions
G. Pts should not take any meds including OTC w/o checking w/dr
H. pts should report blurred vision, persistent headache, dry mouth, dizziness, edema, fainting, weight gain of over 2 lbs/day or 5lbs/week, pulse over 60 and dyspnea
I. fainitng from vasodilation and hypotension w/ alcohol consumption & hot baths
J. teach pts to change positions slowly
K. keep records of angina attacks incl: precipitating factors, number of pills taken, and therapeutic effects
For all: monitor for adverse reactions & therapeutic effects
I Types
A. verapamil (calan)
B. diltiazem (Cardizem)
C. nifedipine (Procardia)
II Mechanism of Action
A. Cause peripheral arterial vasodilation
B. reduce myocardial contractility (negative inotropic action)
C. result: decreased myocardial O2 demand
III Indications
A. First line agents for tx of angina, HPN and supraventricular tachy arryth
B. short term mgmt of atrial fibrillation and flutter
IV Side effects
A. very acceptable side effects and safety profile
B. may cause:
1. hypotension
2. palpitations
3. tachycardia or bradycardia
4. constipation
5. nausea
6. dyspnea
V Nursing implications
A. blood levels should be monitored to ensure they are therapeutic
B. oral CCBs should be taken before meals and as ordered
C. pts should be encouraged to limit caffeine intake
D. before administering, perform a complete health history to determine presence of conditions that may be contraindications for use or call for cautious use
E. obtain baseline VS, including respiratory patterns and rate
F. access for drug interactions
G. Pts should not take any meds including OTC w/o checking w/dr
H. pts should report blurred vision, persistent headache, dry mouth, dizziness, edema, fainting, weight gain of over 2 lbs/day or 5lbs/week, pulse over 60 and dyspnea
I. fainitng from vasodilation and hypotension w/ alcohol consumption & hot baths
J. teach pts to change positions slowly
K. keep records of angina attacks incl: precipitating factors, number of pills taken, and therapeutic effects
For all: monitor for adverse reactions & therapeutic effects
Beta Blockers
Beta Blockers
I Available Forms
A. atenolol (Tenormin)
B. metoprolol (Lopressor)
C. propranolol (Inderal)
D. nadolol (Corgard)
II Mechanism of Action
A. decrease hr resulting in decreased myocardial O2 demand and increase O2 delivery to the heart
B. decrease myocardial contractility helps to conserve energy or decrease demand
C. blocks norepinephrine
III Indications
A. angina
B. anti HPN
C. cardioprotective effects, especially after MI
D. some used for migraine headaches
IV Side effects
A. cardiovascular
1. bradycardia
2. hypotension
3. 2nd or 3rd degree heart block
4. heart failure
B. metabolic
1. glucose
2. lipids
C. CNS
1. dizziness
2. fatigue
3. mental depression
4. lethargy
5. drowsiness
6. unusual dreams
D. other
1. impotence
2. wheezing
3. dyspnea w/ non-selective BB
V Nursing implications
A. monitor pulse rate daily and report any rate lower than 60 bpm
B. dizziness or fainting should also be reported
C. constipation is a common problem; instruct pts to take in adequate fluids and eat high fiber foods
D. never abruptly discontinue due to risk of rebound HPN crisis
E. inform pts that these meds are for long term prevention of angina, not immediate relief
I Available Forms
A. atenolol (Tenormin)
B. metoprolol (Lopressor)
C. propranolol (Inderal)
D. nadolol (Corgard)
II Mechanism of Action
A. decrease hr resulting in decreased myocardial O2 demand and increase O2 delivery to the heart
B. decrease myocardial contractility helps to conserve energy or decrease demand
C. blocks norepinephrine
III Indications
A. angina
B. anti HPN
C. cardioprotective effects, especially after MI
D. some used for migraine headaches
IV Side effects
A. cardiovascular
1. bradycardia
2. hypotension
3. 2nd or 3rd degree heart block
4. heart failure
B. metabolic
1. glucose
2. lipids
C. CNS
1. dizziness
2. fatigue
3. mental depression
4. lethargy
5. drowsiness
6. unusual dreams
D. other
1. impotence
2. wheezing
3. dyspnea w/ non-selective BB
V Nursing implications
A. monitor pulse rate daily and report any rate lower than 60 bpm
B. dizziness or fainting should also be reported
C. constipation is a common problem; instruct pts to take in adequate fluids and eat high fiber foods
D. never abruptly discontinue due to risk of rebound HPN crisis
E. inform pts that these meds are for long term prevention of angina, not immediate relief
Anti-Anginal Drugs
Anti-Anginal Drugs
Chapter 23
Angina Pectoris (Chest Pain)
I When the supply of O2 and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle aches.
II The heart requires a large supply of O2 to meet the demands placed on it.
III Types of Angina
A. Chronic stable angina (aka classic or effort)
B. Unstable (aka preinfarction or crescendo)
C. Vasospastic (aka Prinzmetal’s or variant)
III Antianginal Agents
A. Increase blood flow to ischemic heart muscle
B. And/or decrease myocardial O2 demand
C. Minimize the frequency of attacks and decrease the duration and intensity of anginal pain
D. Improve the pts functional capacity w/as few side effects as possible
E. Types
1. Nitrates/Nitrites
2. Beta blockers DO NOT CONSTRICT
3. Calcium Channel Blockers
Chapter 23
Angina Pectoris (Chest Pain)
I When the supply of O2 and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle aches.
II The heart requires a large supply of O2 to meet the demands placed on it.
III Types of Angina
A. Chronic stable angina (aka classic or effort)
B. Unstable (aka preinfarction or crescendo)
C. Vasospastic (aka Prinzmetal’s or variant)
III Antianginal Agents
A. Increase blood flow to ischemic heart muscle
B. And/or decrease myocardial O2 demand
C. Minimize the frequency of attacks and decrease the duration and intensity of anginal pain
D. Improve the pts functional capacity w/as few side effects as possible
E. Types
1. Nitrates/Nitrites
2. Beta blockers DO NOT CONSTRICT
3. Calcium Channel Blockers
Antiemetic and Antinausea Agents
Antiemetic and Antinausea Agents
Chapter 53
Nausea and Vomiting
I Definitions:
A. Nausea: unpleasant feeling that often precedes vomiting
B. Emesis: vomiting. Forcible emptying of gastric, and occasionally, intestinal contents.
C. Antiemetic agents: used to relieve nausea and vomiting
II Pathophysiology
A. Vomiting center (VC): an area in the brain that is responsible for initiating the physiologic events that lead to nausea and vomiting.
B. Chemoreceptor trigger zone (CTZ): sends neurotransmitter signals to the VC.
C. Once the CTZ and VC are stimulated, they initiate the events that trigger the vomiting reflex.
III Neurotransmitter sites in the vomiting pathway
A. ACh acetylcholine: VC in brain, vestibular and labyrinth pathways in inner ear.
B. Dopamine D2: GI tract and CTZ in brain
C. Histamine H2: VC in brain, vestibular and labyrinth pathways in inner ear
D. Prostaglandins PGs: GI tract
E. Serotonin: GI tract, CTZ and VC in brain
Antiemetic Agents
I Anticholinergic agents
A. Mechanism of action
1. Anticholinergic agents: block ACh receptors in the vestibular nuclei and reticular formation
2. bind to and block ACH receptors in the inner ear labyrinth
3. block transmission of nauseating stimuli to CTZ
4. Also block transmission of nauseating stimuli from the reticular formation to the VC
B. Indications
1. motion sicknes
C. Agents
1. scopolamine (ear patch)
II Antihistamine agents:
A. Mechanism of action
1. Block H1 receptors, thereby preventing ACh from binding to receptors in the vestibular nuclei
2. inhibit ACh by binding to H1 receptors
3. prevent cholinergic stimulation in the vestibular and reticular areas, thus preventing N/V.
B. Indications
1. nonproductive cough
2. allergy symptoms
3. sedation
C. Agents
1. dimenhydrinate
2. diphenhydramine
3. meclizine
4. promethazine
III Neuroleptic agents
A. Mechanism of action
1. block dopamine on the CTZ and may also block ACh
B. Indications
1. also used for psychotic disorders
2. intractable hiccups
C. Agents
1. chlorpromazine
2. perphenazine
3. triflupromazine
IV Prokinetic
A. Mechanism of action
1. block dopamine in the CTZ or stimulate ACh receptors in the GI tract
2. Cause CTZ to be desensitized to impulses it receives from the GI tract
3. also stimulate peristalsis GI tract, enhancing emptying of stomach contents
B. Indications
1. GERD
2. delayed gastric emptying
C. Agents
1. metoclopramide
V Serotonin blockers
A. Mechanism of action
1. block serotonin receptors in the GI tract, CTZ and VC
B. Indications
1. N/V for patients receiving chemotherapy and postoperative nausea and vomiting. No other use...just n/v in chemo.
C. Agents
1. dolasetron
2. granisetron
3. ondansetron
VI Tetrahydrocannabinol
A. Mechanism of action
1. have inhibitory affects on the reticular formation, thalamus, and cerebral cortex
2. major psychoactive substance in marijuana
3. inhibitory effects on reticular formation, thalamus, cerebral cortex
4. alter mood and body’s perception of its surroundings
B. Indications
1. N/V associated with chemotherapy, and anorexia associated with weight loss in AIDS pts
VII Nursing Implications
A. Assess complete nausea and vomiting history, including precipitating factors
B. Assess current medications
C. Assess for contraindications and potential drug interactions
D. Many of these agents cause severe drowsiness; warn pts about driving or performing any hazardous tasks
E. Taking antiemetics with alcohol may cause severe CNS depression
F. Teach pts to change position slowly to avoid hypotensive effects
G. For chemo, antiemetics are often given ½ to 3 hours before a chemo agent.
H. Monitor for therapeutic effects
I. Monitor for adverse effects
Many different mechanisms of action.
Most work by blocking one of the vomiting pathways, thus blocking the stimulus that induces vomiting.
Most indications prevent and reduce nausea and vomiting
Side effects stem from their nonselective blockade of various receptors
Can also be used for...
This is used for:
AIDS
Anorexia
etc
Chapter 53
Nausea and Vomiting
I Definitions:
A. Nausea: unpleasant feeling that often precedes vomiting
B. Emesis: vomiting. Forcible emptying of gastric, and occasionally, intestinal contents.
C. Antiemetic agents: used to relieve nausea and vomiting
II Pathophysiology
A. Vomiting center (VC): an area in the brain that is responsible for initiating the physiologic events that lead to nausea and vomiting.
B. Chemoreceptor trigger zone (CTZ): sends neurotransmitter signals to the VC.
C. Once the CTZ and VC are stimulated, they initiate the events that trigger the vomiting reflex.
III Neurotransmitter sites in the vomiting pathway
A. ACh acetylcholine: VC in brain, vestibular and labyrinth pathways in inner ear.
B. Dopamine D2: GI tract and CTZ in brain
C. Histamine H2: VC in brain, vestibular and labyrinth pathways in inner ear
D. Prostaglandins PGs: GI tract
E. Serotonin: GI tract, CTZ and VC in brain
Antiemetic Agents
I Anticholinergic agents
A. Mechanism of action
1. Anticholinergic agents: block ACh receptors in the vestibular nuclei and reticular formation
2. bind to and block ACH receptors in the inner ear labyrinth
3. block transmission of nauseating stimuli to CTZ
4. Also block transmission of nauseating stimuli from the reticular formation to the VC
B. Indications
1. motion sicknes
C. Agents
1. scopolamine (ear patch)
II Antihistamine agents:
A. Mechanism of action
1. Block H1 receptors, thereby preventing ACh from binding to receptors in the vestibular nuclei
2. inhibit ACh by binding to H1 receptors
3. prevent cholinergic stimulation in the vestibular and reticular areas, thus preventing N/V.
B. Indications
1. nonproductive cough
2. allergy symptoms
3. sedation
C. Agents
1. dimenhydrinate
2. diphenhydramine
3. meclizine
4. promethazine
III Neuroleptic agents
A. Mechanism of action
1. block dopamine on the CTZ and may also block ACh
B. Indications
1. also used for psychotic disorders
2. intractable hiccups
C. Agents
1. chlorpromazine
2. perphenazine
3. triflupromazine
IV Prokinetic
A. Mechanism of action
1. block dopamine in the CTZ or stimulate ACh receptors in the GI tract
2. Cause CTZ to be desensitized to impulses it receives from the GI tract
3. also stimulate peristalsis GI tract, enhancing emptying of stomach contents
B. Indications
1. GERD
2. delayed gastric emptying
C. Agents
1. metoclopramide
V Serotonin blockers
A. Mechanism of action
1. block serotonin receptors in the GI tract, CTZ and VC
B. Indications
1. N/V for patients receiving chemotherapy and postoperative nausea and vomiting. No other use...just n/v in chemo.
C. Agents
1. dolasetron
2. granisetron
3. ondansetron
VI Tetrahydrocannabinol
A. Mechanism of action
1. have inhibitory affects on the reticular formation, thalamus, and cerebral cortex
2. major psychoactive substance in marijuana
3. inhibitory effects on reticular formation, thalamus, cerebral cortex
4. alter mood and body’s perception of its surroundings
B. Indications
1. N/V associated with chemotherapy, and anorexia associated with weight loss in AIDS pts
VII Nursing Implications
A. Assess complete nausea and vomiting history, including precipitating factors
B. Assess current medications
C. Assess for contraindications and potential drug interactions
D. Many of these agents cause severe drowsiness; warn pts about driving or performing any hazardous tasks
E. Taking antiemetics with alcohol may cause severe CNS depression
F. Teach pts to change position slowly to avoid hypotensive effects
G. For chemo, antiemetics are often given ½ to 3 hours before a chemo agent.
H. Monitor for therapeutic effects
I. Monitor for adverse effects
Many different mechanisms of action.
Most work by blocking one of the vomiting pathways, thus blocking the stimulus that induces vomiting.
Most indications prevent and reduce nausea and vomiting
Side effects stem from their nonselective blockade of various receptors
Can also be used for...
This is used for:
AIDS
Anorexia
etc
Laxatives
Laxatives
Drugs that are used to treat constipation.
Constipation
I definition:
A. abnormally infrequent and difficult passage of feces through the lower GI tract
B. A symptom, not a disease
C. Disorder of movement through the colon and/or rectum
D. Can be caused by a variety of disease or drugs
II Causes
A. Adverse drug effects
1. analgesics, anticholinergics, iron supplements, aluminum antacids, calcium antacids, opiates, calcium channel blockers, vinca alkaloids
B. lifestyle
1. poor bowel movement habits: voluntary refusal to defecate
2. diet: poor fluid intake and/or low-residue diets or excessive consumption of dairy products
3. physical inactivity: lack of proper exercise, especially in elderly individuals
4. psychologic: anxiety, stress, hypochondria
C. metabolic and endocrine disorders
1. diabetes mellitus, hypothyroidism, pregnancy, hypercalcemia, hypokalemia
D. neurogenic disorders: autonomic neuropathy, intestinal pseudo-obstruction, multiple sclerosis, spinal cord lesions, Parkinson’s, stroke
Laxatives
I Bulk Forming
A. Mechanism of Action
1. high fiber: safest, can take every day
2. absorbs water to increase bulk
3. distends bowel to initiate reflex bowel activity
B. Side Effects
1. impaction
2. fluid overload
C. Interactions
D. Indications
1. acute and chronic constipation
2. IBS
3. diverticulosis
E. Agents
1. psyllium (Metamucil)
2. polycarbophil
3. methylcellulose (Citrucel)
II Emollient
A. Mechanism of Action
1. stool softeners and lubricants
2. promote more water and fat in the stools
3. lubricate the fecal material and intestinal walls
B. Side Effects
1. skin rashes
2. decreased absorption of vitamins
C. Interactions
D. Indications
1. acute and chronic constipation
2. softening of fecal impacts
3. facilitation of bm’s in anorectal conditions
4. Cardiac pts are on these meds to keep vagal nerve from being stimulated
E. Agents
1. docusate salts (stool softeners) Colace, Surfak
2. mineral oil (lubricants)
III Hyperosmotic
A. Mechanism of Action
1. increase fecal water content
2. result: bowel distention, increased peristalsis, and evacuation
B. Side Effects
1. abdominal bloating
2. rectal irritation
C. Interactions
D. Indications
1. chronic constipation
2. diagnostic and surgical preps
E. Agents
1. polyethylene glycol (goLYTELY) used in bowel preps
2. lactulose (Chronulac)
3. sorbitol
4. glycerin
IV Saline
A. Mechanism of Action
1. similar to hyperosmotic
2. increase osmotic pressure within the intestinal tract causing more water to enter the intestines
3. result: bowel distention, increased peristalsis, and evacuation
B. Side Effects
1. magnesium toxicity (with renal insufficiency) be careful w/kidney disease pts
2. cramping
3. diarrhea
4. increased thirst
C. Interactions
D. Indications
1. constipation (causes a lot of water loss, so not used daily)
2. removal of helminths and parasites
3. diagnostic and surgical bowel prep
E. Agents
1. magnesium sulfate (Epsom salts) bowel preps
2. magnesium phosphate (Fleet Phospho-Soda, Fleet enema) bowel preps
3. magnesium citrate, used for bowel preps
4. magnesium hydroxide (MOM) used for elderly pts
V Stimulant
A. Mechanism of Action
1. increases peristalsis via intestinal nerve stimulation
B. Side Effects
1. addiction can occur
2. nutrient malabsorption
3. skin rashes
4. gastric irritation
5. rectal irritation
C. Interactions
D. Indications
1. acute constipation * only for acute
2. diagnostic and surgical bowel prep
E. Agents
1. castor oil
2. senna
3. anthraquinones
4. cascara
5. bisacodyl
VI Nursing Implications
A. Pts should not take a laxative or cathartic if they are experiencing nausea, vomiting, and/or abdominal pain.
B. long term use of laxatives often results in decreased bowel tone and may lead to dependency
C. All laxative tablets should be swallowed whole, not crushed or chewed, especially if enteric coated
D. All laxatives can cause electrolyte imbalances
E. Bisacodyl and cascara sagrada should be given with water due to interactions with milk, antacids, and H2 blockers. (may open too soon with other liquids)
F. Pts should contact their MD if they experience severe abd pain, muscle weakness, cramps, and/or dizziness, which may indicate possible fluid or electrolyte loss.
G. Monitor for therapeutic effect.
Drugs that are used to treat constipation.
Constipation
I definition:
A. abnormally infrequent and difficult passage of feces through the lower GI tract
B. A symptom, not a disease
C. Disorder of movement through the colon and/or rectum
D. Can be caused by a variety of disease or drugs
II Causes
A. Adverse drug effects
1. analgesics, anticholinergics, iron supplements, aluminum antacids, calcium antacids, opiates, calcium channel blockers, vinca alkaloids
B. lifestyle
1. poor bowel movement habits: voluntary refusal to defecate
2. diet: poor fluid intake and/or low-residue diets or excessive consumption of dairy products
3. physical inactivity: lack of proper exercise, especially in elderly individuals
4. psychologic: anxiety, stress, hypochondria
C. metabolic and endocrine disorders
1. diabetes mellitus, hypothyroidism, pregnancy, hypercalcemia, hypokalemia
D. neurogenic disorders: autonomic neuropathy, intestinal pseudo-obstruction, multiple sclerosis, spinal cord lesions, Parkinson’s, stroke
Laxatives
I Bulk Forming
A. Mechanism of Action
1. high fiber: safest, can take every day
2. absorbs water to increase bulk
3. distends bowel to initiate reflex bowel activity
B. Side Effects
1. impaction
2. fluid overload
C. Interactions
D. Indications
1. acute and chronic constipation
2. IBS
3. diverticulosis
E. Agents
1. psyllium (Metamucil)
2. polycarbophil
3. methylcellulose (Citrucel)
II Emollient
A. Mechanism of Action
1. stool softeners and lubricants
2. promote more water and fat in the stools
3. lubricate the fecal material and intestinal walls
B. Side Effects
1. skin rashes
2. decreased absorption of vitamins
C. Interactions
D. Indications
1. acute and chronic constipation
2. softening of fecal impacts
3. facilitation of bm’s in anorectal conditions
4. Cardiac pts are on these meds to keep vagal nerve from being stimulated
E. Agents
1. docusate salts (stool softeners) Colace, Surfak
2. mineral oil (lubricants)
III Hyperosmotic
A. Mechanism of Action
1. increase fecal water content
2. result: bowel distention, increased peristalsis, and evacuation
B. Side Effects
1. abdominal bloating
2. rectal irritation
C. Interactions
D. Indications
1. chronic constipation
2. diagnostic and surgical preps
E. Agents
1. polyethylene glycol (goLYTELY) used in bowel preps
2. lactulose (Chronulac)
3. sorbitol
4. glycerin
IV Saline
A. Mechanism of Action
1. similar to hyperosmotic
2. increase osmotic pressure within the intestinal tract causing more water to enter the intestines
3. result: bowel distention, increased peristalsis, and evacuation
B. Side Effects
1. magnesium toxicity (with renal insufficiency) be careful w/kidney disease pts
2. cramping
3. diarrhea
4. increased thirst
C. Interactions
D. Indications
1. constipation (causes a lot of water loss, so not used daily)
2. removal of helminths and parasites
3. diagnostic and surgical bowel prep
E. Agents
1. magnesium sulfate (Epsom salts) bowel preps
2. magnesium phosphate (Fleet Phospho-Soda, Fleet enema) bowel preps
3. magnesium citrate, used for bowel preps
4. magnesium hydroxide (MOM) used for elderly pts
V Stimulant
A. Mechanism of Action
1. increases peristalsis via intestinal nerve stimulation
B. Side Effects
1. addiction can occur
2. nutrient malabsorption
3. skin rashes
4. gastric irritation
5. rectal irritation
C. Interactions
D. Indications
1. acute constipation * only for acute
2. diagnostic and surgical bowel prep
E. Agents
1. castor oil
2. senna
3. anthraquinones
4. cascara
5. bisacodyl
VI Nursing Implications
A. Pts should not take a laxative or cathartic if they are experiencing nausea, vomiting, and/or abdominal pain.
B. long term use of laxatives often results in decreased bowel tone and may lead to dependency
C. All laxative tablets should be swallowed whole, not crushed or chewed, especially if enteric coated
D. All laxatives can cause electrolyte imbalances
E. Bisacodyl and cascara sagrada should be given with water due to interactions with milk, antacids, and H2 blockers. (may open too soon with other liquids)
F. Pts should contact their MD if they experience severe abd pain, muscle weakness, cramps, and/or dizziness, which may indicate possible fluid or electrolyte loss.
G. Monitor for therapeutic effect.
Antidiarrheals
Antidiarrheals
Drugs that are used to treat diarrhea.
Diarrhea
I Definition: Abnormal frequent passage of loose stools or abnormal passage of stools with increased frequency, fluidity, and weight. Or with increased stool water excretion.
A. acute:
1. sudden onset in a previously healthy person
2. lasts from 3 days to 2 weeks
3. self-limiting
4. resolves without sequelae
5. causes
a. bacterial
b. viral
c. drug induced
d. nutritional
e. protozoal
B. chronic
1. lasts for more than 3 weeks
2. associated with recurring passage of diarrheal stools, fever, loss of appetite, nausea, vomiting, weight loss, and chronic weakness
3. causes
a. tumors
b. diabetes
c. Addison’s disease
d. hyperthroidism
e. irritable bowel syndrome (IBS)
Antidiarrheals
I Adsorbents
A. Mechanism of action
1. act by coating the walls of the GI tract.
2. bind the causative bacteria or toxin to their adsorbent surface for elimination from the body through the stool
3. ex: bismuth subsalicylate (pepto-bismol). This agent is in an “aspirin-like” compound.
B. Side effects
1. increased bleeding time (anti-coagulant, not a blood thinner)
2. constipation
3. dark stools
4. confusion
5. twitching
6. hearing loss, tinnitus
7. metallic taste
8. blue gums
C. Interactions
1. adsorbents decrease the absorption of many agents including: digoxin, clindamycin, quinidine, and hypoglycemic agents.
2. adsorbents cause increased bleeding time when given with anticoagulants.
D. Agents
1. activated charcoal
2. aluminum hydroxide
3. attapulgite
4. bismuth subsalicylate
5. cholestyramine
6. kaolin-pectin
7. polycarbonphil
****Do not give bismuth subsalicylate to children younger than 16 or teenagers with chicken pox because of the risk of Reye’s syndrome.
II Anticholinergics
A. Mechanism of action
1. decrease intestinal muscle tone and peristalsis of GI tract
2. result: slowing the movement of fecal matter through the GI tract
3. examples:
a. belladonna alkaloids (Donnatal)
b. atropine
c. hyoscyamine
B. Side effects
1. urinary retention, hesitancy
2. impotence
3. headache, dizziness, confusion, anxiety, drowsiness
4. dry skin, rash, flushing
5. blurred vision, photophobia, increased intraocular pressure
6. hypotension, hypertension, bradycardia, tachycardia
C. Indications
1. antacids can decrease effects of anticholinergic antidiarrheal agents.
D. Agents
1. atropine
2. hyoscyamine
3. hyoscine
*** Anticholinergics should not be administered to patients with a history of glaucoma, BPH, urinary retention, recent bladder surgery, cardiac problems, or myasthenia gravis. It will make them worse.
III Intestinal Flora Modifiers
A. Mechanism of action
1. bacterial cultures of Lactobacillus organisms. Work by:
a. supplying missing bacteria to the GI tract
b. suppressing the growth of diarrhea-causing bacteria
2. example: L. acidophilus (Lactinex) Used after a course of antibiotics.
B. side effects: mild
C. Indications
D. Agents
1. Lactobacillus acidophilus
IV Opiates
A. Mechanism of action
1. decrease bowel motility and relieve rectal spasms
2. decrease transit time through the bowel, allowing more time for water and electrolytes to be absorbed.
3. examples:
a. paregoric
b. opium tincture
c. codeine
d. loperamide (Imodium)
e. diphenoxylate (Lomotil)
f. vicodin/hydrocodone
4. Opiates cause constipation in all of our patients
B. Side effects: (some similarities to antcholinergic)
1. drowsiness, sedation, dizziness, lethargy
2. nausea, vomiting, anorexia, constipation
3. respiratory depression
4. bradycardia, palpitations, hypotension
5. urinary retention
6. flushing, rash, urticaria
7. addiction (not Immodium)
C. Agents
1. opium tincture
2. paregoric
3. codeine
4. diphenoxylate (Lomotil)
5. loperamide (Immodium)
6. morphine
***
Opiates have some similarities to anticholinergic drugs
Contraindicated for pts on anti-coagulants
Any liquid med, do not give with other meds. Changes the pH of the stomach.
Drugs that are used to treat diarrhea.
Diarrhea
I Definition: Abnormal frequent passage of loose stools or abnormal passage of stools with increased frequency, fluidity, and weight. Or with increased stool water excretion.
A. acute:
1. sudden onset in a previously healthy person
2. lasts from 3 days to 2 weeks
3. self-limiting
4. resolves without sequelae
5. causes
a. bacterial
b. viral
c. drug induced
d. nutritional
e. protozoal
B. chronic
1. lasts for more than 3 weeks
2. associated with recurring passage of diarrheal stools, fever, loss of appetite, nausea, vomiting, weight loss, and chronic weakness
3. causes
a. tumors
b. diabetes
c. Addison’s disease
d. hyperthroidism
e. irritable bowel syndrome (IBS)
Antidiarrheals
I Adsorbents
A. Mechanism of action
1. act by coating the walls of the GI tract.
2. bind the causative bacteria or toxin to their adsorbent surface for elimination from the body through the stool
3. ex: bismuth subsalicylate (pepto-bismol). This agent is in an “aspirin-like” compound.
B. Side effects
1. increased bleeding time (anti-coagulant, not a blood thinner)
2. constipation
3. dark stools
4. confusion
5. twitching
6. hearing loss, tinnitus
7. metallic taste
8. blue gums
C. Interactions
1. adsorbents decrease the absorption of many agents including: digoxin, clindamycin, quinidine, and hypoglycemic agents.
2. adsorbents cause increased bleeding time when given with anticoagulants.
D. Agents
1. activated charcoal
2. aluminum hydroxide
3. attapulgite
4. bismuth subsalicylate
5. cholestyramine
6. kaolin-pectin
7. polycarbonphil
****Do not give bismuth subsalicylate to children younger than 16 or teenagers with chicken pox because of the risk of Reye’s syndrome.
II Anticholinergics
A. Mechanism of action
1. decrease intestinal muscle tone and peristalsis of GI tract
2. result: slowing the movement of fecal matter through the GI tract
3. examples:
a. belladonna alkaloids (Donnatal)
b. atropine
c. hyoscyamine
B. Side effects
1. urinary retention, hesitancy
2. impotence
3. headache, dizziness, confusion, anxiety, drowsiness
4. dry skin, rash, flushing
5. blurred vision, photophobia, increased intraocular pressure
6. hypotension, hypertension, bradycardia, tachycardia
C. Indications
1. antacids can decrease effects of anticholinergic antidiarrheal agents.
D. Agents
1. atropine
2. hyoscyamine
3. hyoscine
*** Anticholinergics should not be administered to patients with a history of glaucoma, BPH, urinary retention, recent bladder surgery, cardiac problems, or myasthenia gravis. It will make them worse.
III Intestinal Flora Modifiers
A. Mechanism of action
1. bacterial cultures of Lactobacillus organisms. Work by:
a. supplying missing bacteria to the GI tract
b. suppressing the growth of diarrhea-causing bacteria
2. example: L. acidophilus (Lactinex) Used after a course of antibiotics.
B. side effects: mild
C. Indications
D. Agents
1. Lactobacillus acidophilus
IV Opiates
A. Mechanism of action
1. decrease bowel motility and relieve rectal spasms
2. decrease transit time through the bowel, allowing more time for water and electrolytes to be absorbed.
3. examples:
a. paregoric
b. opium tincture
c. codeine
d. loperamide (Imodium)
e. diphenoxylate (Lomotil)
f. vicodin/hydrocodone
4. Opiates cause constipation in all of our patients
B. Side effects: (some similarities to antcholinergic)
1. drowsiness, sedation, dizziness, lethargy
2. nausea, vomiting, anorexia, constipation
3. respiratory depression
4. bradycardia, palpitations, hypotension
5. urinary retention
6. flushing, rash, urticaria
7. addiction (not Immodium)
C. Agents
1. opium tincture
2. paregoric
3. codeine
4. diphenoxylate (Lomotil)
5. loperamide (Immodium)
6. morphine
***
Opiates have some similarities to anticholinergic drugs
Contraindicated for pts on anti-coagulants
Any liquid med, do not give with other meds. Changes the pH of the stomach.
Proton Pump Inhibitors
Acid Controlling Agents
Proton Pump Inhibitors: (PPI) The newest drugs introduced for the treatment of acid-related disorders. More powerful than H2 antagonists, they bind directly to the hydrogen-potassium-ATPase pump mechanism. They irreversibly inhibit the action of this enzyme, which results in a total (100% blockage of pump) blockage of hydrogen ion secretion from the parietal cells.
I Definition
A. The parietal cells release positive hydrogen ions (protons) during HCl production
B. This process is called the “proton pump”
C. H2 blockers and antihistamines do not stop the action of this pump
II Mechanism of action (pg 797)
A. Irreversibly bind to h+/k+ ATPase enzyme
B. This bond prevents the movement of hydrogen ions from the pariental cell into the stomach
C. Result: achlorhydria – ALL gastric acid secretion is blocked
1. in order to return to normal acid secretion, the parietal cell must synthesize new H+/K+ ATPase.
III Drug Effect
A. Total inhibition of gastric acid secretion
1. lansoprazole (prevacid)
2. omeprazole (prilosec)...first in this new class
3. pantoprazole (protonix) IV
4. esomeprazole (nexium) IV
IV Indications
A. GERD maintenance therapy
B. Erosive esophagitis
C. Short-term treatment of active duodenal and benign gastric ulcers
D. Zollinger-Ellison syndrome (hypersecretory)
E. Treatment of H. pylori induced ulcers
V Side Effects
A. Safe for short term therapy
B. incidence low and uncommon (pretty nil)
VI Nursing Implications
A. Assess for allergies and history of liver disease
B. Pantoprazole is the only proton pump inhibitor available for parenteral administration, and can be used for patients who are unable to take oral medications (also esomeprazole) Nexium
C. May increase serum levels of diazepam, phenytoin, and cause increased chance for bleeding with warfarin.
D. In the patient taking omeprazole:
1. take before meals (empty stomach)
2. the capsule needs to be swallowed whole, not crushed, opened, or chewed
3. it may be given with antacids
4. emphasize that the treatment will be short term
Other Drugs
I Sucralfate (Carafate)
A. Cytoprotective agent
B. used for stress ulcers, erosions, PUD
C. Attracted to and binds to the base of ulcers and erosions forming a protective barrier over these areas
D. Protects these areas from pepsin, which normally breaks down proteins (making ulcers worse)
E. Not an antacid works like a band aid
F. Little absorption from the gut
G. May cause constipation, nausea, and dry mouth
H. May impair absorption of other drugs, especially tetracycline. Give alone
I. Binds with phosphate, may be used in chronic renal failure to reduce phosphate levels.
J. Do not administer with other medications.
II Misoprostol (Cytotec)
A. Synthetic prostaglandin analog
B. Prostaglandins have cytoprotective activity
1. protect gastric mucosa from injury (ulcers) by enhancing local production of mucus or bicarbonate. (Helps protect stomach from ulcers caused by NSAIDS)
2. promote local cell regeneration
3. help to maintain mucosal blood flow
C. Used for prevention of NSAID induced gastric ulcers
D. Doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps, diarrhea
E. used to induce labor...pregnant women should not handle
Proton Pump Inhibitors: (PPI) The newest drugs introduced for the treatment of acid-related disorders. More powerful than H2 antagonists, they bind directly to the hydrogen-potassium-ATPase pump mechanism. They irreversibly inhibit the action of this enzyme, which results in a total (100% blockage of pump) blockage of hydrogen ion secretion from the parietal cells.
I Definition
A. The parietal cells release positive hydrogen ions (protons) during HCl production
B. This process is called the “proton pump”
C. H2 blockers and antihistamines do not stop the action of this pump
II Mechanism of action (pg 797)
A. Irreversibly bind to h+/k+ ATPase enzyme
B. This bond prevents the movement of hydrogen ions from the pariental cell into the stomach
C. Result: achlorhydria – ALL gastric acid secretion is blocked
1. in order to return to normal acid secretion, the parietal cell must synthesize new H+/K+ ATPase.
III Drug Effect
A. Total inhibition of gastric acid secretion
1. lansoprazole (prevacid)
2. omeprazole (prilosec)...first in this new class
3. pantoprazole (protonix) IV
4. esomeprazole (nexium) IV
IV Indications
A. GERD maintenance therapy
B. Erosive esophagitis
C. Short-term treatment of active duodenal and benign gastric ulcers
D. Zollinger-Ellison syndrome (hypersecretory)
E. Treatment of H. pylori induced ulcers
V Side Effects
A. Safe for short term therapy
B. incidence low and uncommon (pretty nil)
VI Nursing Implications
A. Assess for allergies and history of liver disease
B. Pantoprazole is the only proton pump inhibitor available for parenteral administration, and can be used for patients who are unable to take oral medications (also esomeprazole) Nexium
C. May increase serum levels of diazepam, phenytoin, and cause increased chance for bleeding with warfarin.
D. In the patient taking omeprazole:
1. take before meals (empty stomach)
2. the capsule needs to be swallowed whole, not crushed, opened, or chewed
3. it may be given with antacids
4. emphasize that the treatment will be short term
Other Drugs
I Sucralfate (Carafate)
A. Cytoprotective agent
B. used for stress ulcers, erosions, PUD
C. Attracted to and binds to the base of ulcers and erosions forming a protective barrier over these areas
D. Protects these areas from pepsin, which normally breaks down proteins (making ulcers worse)
E. Not an antacid works like a band aid
F. Little absorption from the gut
G. May cause constipation, nausea, and dry mouth
H. May impair absorption of other drugs, especially tetracycline. Give alone
I. Binds with phosphate, may be used in chronic renal failure to reduce phosphate levels.
J. Do not administer with other medications.
II Misoprostol (Cytotec)
A. Synthetic prostaglandin analog
B. Prostaglandins have cytoprotective activity
1. protect gastric mucosa from injury (ulcers) by enhancing local production of mucus or bicarbonate. (Helps protect stomach from ulcers caused by NSAIDS)
2. promote local cell regeneration
3. help to maintain mucosal blood flow
C. Used for prevention of NSAID induced gastric ulcers
D. Doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps, diarrhea
E. used to induce labor...pregnant women should not handle
H2 Antagonists
Acid Controlling Agents
H2 antagonists (aka H2 receptor blockers): reduce but do not abolish stimulated acid secretion. They have become the most popular drugs for the treatment of many acid-related disorders including PUD. Available OTC in lower dosage forms. Cimedidine (Tagament), famotidine (pepcid), ranitidine (zantac), nizatidine. There is little difference among the 4 available drugs.
I Mechanism of action
A. Completely block histamine (H2) at the receptors of acid producing parietal cells
B. production of hydrogen ions is reduced, resulting in decreased production of HCl. This results in an increase in the pH of the stomach and relief of many of the symptoms associated with hyperacidity-related conditions.
II Drug Effect
A. Suppressed acid secretion in the stomach
III Indications: several therapeutic uses including treatment of:
A. GERD
B. PUD
C. erosive esophagitis
D. Adjunct therapy in control of upper GI bleeding
E. pathologic gastric hypersecretory conditions
IV Contraindications: known allergy
V Side effects:
A. overall, less than 3% incidence of side effects
B. Cimetidine may induce impotence and gynecomastia
C. May see: headaches, lethargy, confusion, diarrhea, urticaria, sweating, flushing, other
VI Interactions
A. Cimetidine carries a higher risk of drug interactions than the other three HA’s.
1. binds with P-450 microsomal oxidase system in the liver, resulting in inhibited oxidation of many drugs and increased drug levels.
B. All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for absorption
C. Smoking has been shown to decrease the effectiveness of H2 blockers.
VII Nursing Implications
A. Assess for allergies and impaired renal of liver function.
B. Use with caution in patients who are confused, disoriented, or elderly
C. Take 1 hour before or after antacids
D. For intravenous doses, follow administration guidelines
H2 antagonists (aka H2 receptor blockers): reduce but do not abolish stimulated acid secretion. They have become the most popular drugs for the treatment of many acid-related disorders including PUD. Available OTC in lower dosage forms. Cimedidine (Tagament), famotidine (pepcid), ranitidine (zantac), nizatidine. There is little difference among the 4 available drugs.
I Mechanism of action
A. Completely block histamine (H2) at the receptors of acid producing parietal cells
B. production of hydrogen ions is reduced, resulting in decreased production of HCl. This results in an increase in the pH of the stomach and relief of many of the symptoms associated with hyperacidity-related conditions.
II Drug Effect
A. Suppressed acid secretion in the stomach
III Indications: several therapeutic uses including treatment of:
A. GERD
B. PUD
C. erosive esophagitis
D. Adjunct therapy in control of upper GI bleeding
E. pathologic gastric hypersecretory conditions
IV Contraindications: known allergy
V Side effects:
A. overall, less than 3% incidence of side effects
B. Cimetidine may induce impotence and gynecomastia
C. May see: headaches, lethargy, confusion, diarrhea, urticaria, sweating, flushing, other
VI Interactions
A. Cimetidine carries a higher risk of drug interactions than the other three HA’s.
1. binds with P-450 microsomal oxidase system in the liver, resulting in inhibited oxidation of many drugs and increased drug levels.
B. All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for absorption
C. Smoking has been shown to decrease the effectiveness of H2 blockers.
VII Nursing Implications
A. Assess for allergies and impaired renal of liver function.
B. Use with caution in patients who are confused, disoriented, or elderly
C. Take 1 hour before or after antacids
D. For intravenous doses, follow administration guidelines
Antacids
Acid Controlling Agents
Antacids
I. Mechanism of Action
A. promote gastric mucosal defense mechanisms
1. secretion of:
a. mucus: protective barrier against HCl
b. bicarbonate: helps buffer acidic properties of HCL
c. prostaglandins: prevent activation of proton pump
B. antacids DO NOT prevent the overproduction of acid
C. antacids DO neutralize the acid once it is in the stomach (only neutralize, don’t prevent)
D. Work primarily by neutralizing gastric acidity.
E. Reduction of pain associated with acid related disorders
1. raising gastric pH from 1.3 to 1.6 neutralizes 50% of gastric acid
2. raising gastric pH 1 point (1.3 to 2.3) neutralizes 90% of gastric acid
3. reducing acidity, reduces pain
II. Indications
A. indicated for the acute relief of symptoms associated with peptic ulcer, gastritis, gastric hyperacidity, and heartburn.
III. Contraindications
A. known allergy
B. severe renal failure or electrolyte disturbances
IV. Drug profiles
A. OTC formulations available as:
1. capsules and tablets
2. powders
3. chewable tablets
4. suspensions
5. effervescent granules and tablets
V. antacids can be used alone or in combination with:
A. aluminum salts
1. forms: carbonate, hydroxide
2. have constipating effects
3. often used with magnesium to counteract constipation
4. examples:
a. aluminum carbonate (Basaljel)
b. Hydroxide salt (Alterna GEL)
c. Combination products: (alum & magn) Gaviscon, Maalox, Mylanta, DiGel
B. magnesium salts
1. forms: carbonate, hydroxide, oxide, trisilicate
2. commonly cause diarrhea, usually used with other agents to counteract this effect
3. DANGEROUS when used with renal failure. The failing kidney cannot excrete extra magnesium, resulting in accumulation
4. examples:
a. hydroxide salt (magnesium hydroxide) MOM
b. carbonate salt (combination) Gaviscon
c. combination products: (alum & magn) Maalox, mylanta
C. calcium salts
1. may cause constipation
2. their use may result in kidney stones
3. long duration of acid action may cause increased gastric acid secretion (hyperacidity rebound)
4. often advertised as an extra source of calcium (Tums)
D. sodium bicarbonate
1. highly soluble
2. buffers the acidic properties of HCl
3. quick onset, but short duration
4. may cause metabolic alkalosis
5. sodium content may cause problems in patients with HF, HTN, or renal insufficiency
VI. Antacids and antiflatulents
A. used to relieve the painful symptoms associated with gas
B. several agents are used to bind or alter intestinal gas and are often added to antacid combination products
C. simethicone (mylicon)
1. alters elasticity of mucus-coated bubbles, causing them to break
2. used often, but there are limited data to support effectiveness
VII. Antacid side effects, are minimal and depend on the compound used
A. Alum & calcium: constipation
B. magnesium: diarrhea
C. calcium carbonate: produces gas and belching, often combined with simethicone.
VIII. Drug interactions
A. adsorption of other drugs to antacids (**do NOT administer with other drugs)
1. reduces the ability of the other drug to be absorbed into the body
B. chelation
1. chemical binding, or inactivation, of another drug
2. produces insoluble complexes
3. result: reduced drug absorption
C. Increased stomach pH
1. increased absorption of basic drugs
2. decreased absorption of acidic drugs
D. Increased urinary pH (opposite)
1. increased excretion of acidic drugs
2. decreased excretion of basic drugs
IX. Nursing Implications
A. Use with caution with other medications due to the many drug interactions
B. Most medications should be given 2-3 hours after giving an antacid
C. Antacids may cause premature dissolving of enteric-coated medication, resulting in stomach upset
D. Be sure that chewable tablets are chewed thoroughly, and liquid forms are shaken well before giving.
E. Administer with at least 8 oz of H2O to enhance absorption (except for rapid dissolve forms)
F. Caffeine, alcohol, harsh spices, and black pepper may aggravate the underlying GI condition
G. Monitor side effects:
1. nausea, vomiting, abd pain, diarrhea
2. with calcium containing products: constipation and acid rebound
H. Monitor for therapeutic response
1. notify health care provider if symptoms are not relieved
I. Assess for allergies and preexisting conditions that may restrict the use of antacids, such as:
1. fluid imbalances, renal disease, heart failure
2. pregnancy
3. GI obstruction
J. Pts with heart failure or HPN should use low-sodium antacids such as Riopan, Maalox, or Mylanta II.
Which of the following would we give to a:
Renal insufficient patient? Basajel (aluminum salt alone)
A female who require extra calcium? Tums
A 33 y/o male suffering from gastric acidity (a regular person)? Mylanta/Maalox
What is true of sodium bicarbonate?
Should be used sparingly in renal insufficiency.
Antacids
I. Mechanism of Action
A. promote gastric mucosal defense mechanisms
1. secretion of:
a. mucus: protective barrier against HCl
b. bicarbonate: helps buffer acidic properties of HCL
c. prostaglandins: prevent activation of proton pump
B. antacids DO NOT prevent the overproduction of acid
C. antacids DO neutralize the acid once it is in the stomach (only neutralize, don’t prevent)
D. Work primarily by neutralizing gastric acidity.
E. Reduction of pain associated with acid related disorders
1. raising gastric pH from 1.3 to 1.6 neutralizes 50% of gastric acid
2. raising gastric pH 1 point (1.3 to 2.3) neutralizes 90% of gastric acid
3. reducing acidity, reduces pain
II. Indications
A. indicated for the acute relief of symptoms associated with peptic ulcer, gastritis, gastric hyperacidity, and heartburn.
III. Contraindications
A. known allergy
B. severe renal failure or electrolyte disturbances
IV. Drug profiles
A. OTC formulations available as:
1. capsules and tablets
2. powders
3. chewable tablets
4. suspensions
5. effervescent granules and tablets
V. antacids can be used alone or in combination with:
A. aluminum salts
1. forms: carbonate, hydroxide
2. have constipating effects
3. often used with magnesium to counteract constipation
4. examples:
a. aluminum carbonate (Basaljel)
b. Hydroxide salt (Alterna GEL)
c. Combination products: (alum & magn) Gaviscon, Maalox, Mylanta, DiGel
B. magnesium salts
1. forms: carbonate, hydroxide, oxide, trisilicate
2. commonly cause diarrhea, usually used with other agents to counteract this effect
3. DANGEROUS when used with renal failure. The failing kidney cannot excrete extra magnesium, resulting in accumulation
4. examples:
a. hydroxide salt (magnesium hydroxide) MOM
b. carbonate salt (combination) Gaviscon
c. combination products: (alum & magn) Maalox, mylanta
C. calcium salts
1. may cause constipation
2. their use may result in kidney stones
3. long duration of acid action may cause increased gastric acid secretion (hyperacidity rebound)
4. often advertised as an extra source of calcium (Tums)
D. sodium bicarbonate
1. highly soluble
2. buffers the acidic properties of HCl
3. quick onset, but short duration
4. may cause metabolic alkalosis
5. sodium content may cause problems in patients with HF, HTN, or renal insufficiency
VI. Antacids and antiflatulents
A. used to relieve the painful symptoms associated with gas
B. several agents are used to bind or alter intestinal gas and are often added to antacid combination products
C. simethicone (mylicon)
1. alters elasticity of mucus-coated bubbles, causing them to break
2. used often, but there are limited data to support effectiveness
VII. Antacid side effects, are minimal and depend on the compound used
A. Alum & calcium: constipation
B. magnesium: diarrhea
C. calcium carbonate: produces gas and belching, often combined with simethicone.
VIII. Drug interactions
A. adsorption of other drugs to antacids (**do NOT administer with other drugs)
1. reduces the ability of the other drug to be absorbed into the body
B. chelation
1. chemical binding, or inactivation, of another drug
2. produces insoluble complexes
3. result: reduced drug absorption
C. Increased stomach pH
1. increased absorption of basic drugs
2. decreased absorption of acidic drugs
D. Increased urinary pH (opposite)
1. increased excretion of acidic drugs
2. decreased excretion of basic drugs
IX. Nursing Implications
A. Use with caution with other medications due to the many drug interactions
B. Most medications should be given 2-3 hours after giving an antacid
C. Antacids may cause premature dissolving of enteric-coated medication, resulting in stomach upset
D. Be sure that chewable tablets are chewed thoroughly, and liquid forms are shaken well before giving.
E. Administer with at least 8 oz of H2O to enhance absorption (except for rapid dissolve forms)
F. Caffeine, alcohol, harsh spices, and black pepper may aggravate the underlying GI condition
G. Monitor side effects:
1. nausea, vomiting, abd pain, diarrhea
2. with calcium containing products: constipation and acid rebound
H. Monitor for therapeutic response
1. notify health care provider if symptoms are not relieved
I. Assess for allergies and preexisting conditions that may restrict the use of antacids, such as:
1. fluid imbalances, renal disease, heart failure
2. pregnancy
3. GI obstruction
J. Pts with heart failure or HPN should use low-sodium antacids such as Riopan, Maalox, or Mylanta II.
Which of the following would we give to a:
Renal insufficient patient? Basajel (aluminum salt alone)
A female who require extra calcium? Tums
A 33 y/o male suffering from gastric acidity (a regular person)? Mylanta/Maalox
What is true of sodium bicarbonate?
Should be used sparingly in renal insufficiency.
Acid Controlling Drugs Pathology
Acid Controlling Drugs Pathology
Chapter 51
Pathophysiology
Definitions:
HCL: an acid that aids digestion and also serves as a barrier to infection
Bicarbonate: a base that is a natural mechanism to prevent hyperacidity
Pepsinogen: an enzymatic precursor to pepsin, an enzyme that digests dietary proteins
Intrinsic factor: a glycoprotein that facilitates gastric absorption of vit B12
Mucus: for protection of the stomach lining from both HCl and digestive enzymes
Prostaglandins (PGs): have a variety of antiinflamatory and protective functions.
I The stomach can be divided into three functional areas. Each area has specific glands with which it is associated. These glands are composed of different cells which secrete different substances.
A. Cardiac:
B. Fundic/gastric:
1. most numerous
2. of primary importance to the discussion of acid-related disorders and drug therapy.
3. Highly specialized secretory glands composed of several different types of cells.
a. parietal: (see fig. 49-2)
i. produce and secrete HCl
ii. pimary site of action for many acid controlling drugs
b. chief:
i. secrete pepsinogen, a proenzyme
ii. pepsinogen becomes pepsin when activated by exposure to acid
iii. pepsin breaks down proteins (proteolytic)
c. mucoid/mucous:
i. mucus secreting cells (surface epithelial cells)
ii. provide a protective mucous coat
iii. protect against self-digestion by HCl
d. endocrine
e. enterochromaffin
C. pyloric:
II When the three main gastric cells or their secretions are impaired, acid related diseases can occur.
A. hypersecretion
1. the most harmful of the acid related diseases
2. include:
a. peptic ulcer disease (PUD)
b. esophageal cancer
B. mild to moderate hyperacidity
1. most common condition
2. overproduction of HCl by the parietal cells
3. include:
a. indigestion, sour stomach, heartburn, acid stomach
b. GERD
C. Helicobacter pylori is a contagious diseases.
1. bacteria found in GI tract of 90% of patients with duodenal ulcers and 70% of those with gastric ulcers
2. antibiotics are used to eradicate (tetracycline)
III Hydrochloric Acid (HCl)
A. Secreted by the parietal cells when stimulated by food
B. Maintains stomach pH of 1 to 4
C. Aids in the proper digestion of food
D. Serves as one of the body’s defenses against infection in GI tract
E. Excretion also stimulated by:
1. large fatty meals
2. excessive amounts of alcohol
3. emotional stress
F. The primary target for many of the most effective drugs for the treatment of acid related disorders.
Chapter 51
Pathophysiology
Definitions:
HCL: an acid that aids digestion and also serves as a barrier to infection
Bicarbonate: a base that is a natural mechanism to prevent hyperacidity
Pepsinogen: an enzymatic precursor to pepsin, an enzyme that digests dietary proteins
Intrinsic factor: a glycoprotein that facilitates gastric absorption of vit B12
Mucus: for protection of the stomach lining from both HCl and digestive enzymes
Prostaglandins (PGs): have a variety of antiinflamatory and protective functions.
I The stomach can be divided into three functional areas. Each area has specific glands with which it is associated. These glands are composed of different cells which secrete different substances.
A. Cardiac:
B. Fundic/gastric:
1. most numerous
2. of primary importance to the discussion of acid-related disorders and drug therapy.
3. Highly specialized secretory glands composed of several different types of cells.
a. parietal: (see fig. 49-2)
i. produce and secrete HCl
ii. pimary site of action for many acid controlling drugs
b. chief:
i. secrete pepsinogen, a proenzyme
ii. pepsinogen becomes pepsin when activated by exposure to acid
iii. pepsin breaks down proteins (proteolytic)
c. mucoid/mucous:
i. mucus secreting cells (surface epithelial cells)
ii. provide a protective mucous coat
iii. protect against self-digestion by HCl
d. endocrine
e. enterochromaffin
C. pyloric:
II When the three main gastric cells or their secretions are impaired, acid related diseases can occur.
A. hypersecretion
1. the most harmful of the acid related diseases
2. include:
a. peptic ulcer disease (PUD)
b. esophageal cancer
B. mild to moderate hyperacidity
1. most common condition
2. overproduction of HCl by the parietal cells
3. include:
a. indigestion, sour stomach, heartburn, acid stomach
b. GERD
C. Helicobacter pylori is a contagious diseases.
1. bacteria found in GI tract of 90% of patients with duodenal ulcers and 70% of those with gastric ulcers
2. antibiotics are used to eradicate (tetracycline)
III Hydrochloric Acid (HCl)
A. Secreted by the parietal cells when stimulated by food
B. Maintains stomach pH of 1 to 4
C. Aids in the proper digestion of food
D. Serves as one of the body’s defenses against infection in GI tract
E. Excretion also stimulated by:
1. large fatty meals
2. excessive amounts of alcohol
3. emotional stress
F. The primary target for many of the most effective drugs for the treatment of acid related disorders.
Cholinergic Drugs
Cholinergic Agents
Chapter 19
I Cholinergic Agents: drugs that stimulate the PSNS (parasympathetic nervous system). The opposing system to the SNS. (seemed to be used in biological warfare)
A. Rest or digest.
B. only one we need to know is ACh.
C. AKA as cholinergic agonists or parasympathomimetics.
D. Mimic the effects of the PSNS neurotransmitter acetylcholine (ACh)
E. 2 types determined by location and action once stimulated
1. Nicotinic receptors
a. Located in the ganglia of both the PSNS and SNS
b. Named “nicotinic” bc can be stimulated by the alkaloid nicotine
2. Muscarinic receptors
a. Located postsynaptically
1. smooth muscle
2. cardiac muscle
3. glands of parasympathetic fibers
4. effector organs of cholinergic sympathetic fibers
b. Can be stimulated by the alkaloid muscarine
II Mechanism of Action
A. Direct acting cholinergic agonists
1. bind to cholinergic receptors, activating them
B. Indirect acting (cholinesterase inhibitors)
1. inhibit the enzyme cholinesterase which breaks down ACh
2. result: more ACh is available at the receptors
3. can be:
a. reversible: bind to cholinesterase for a period of minutes or hours
b. irreversible: bind to cholinesterase and form a permanent covalent bond. The body must make new cholinesterase as in nerve gas damage.
III Drug Effects
A. Effects seen when the PSNS is stimulated
B. The PSNS is the “rest and digest” system
C. SLUDGE (some kind of excretion)
Salivation
Lacrimation (tears)
Urinary incontinence
Diarrhea
Gastrointestinal cramps
Emesis
D. Stimulate intestine and bladder
1. increased gastric secretions
2. increased GI motility
3. increased urinary frequency
E. stimulate pupil
1. contriction (miosis)
2. reduced intraocular pressure (used for glaucoma)
F. increased salivation and sweating
G. Cardiovascular effects
1. decreased heart rate
2. vasoldilation
H. respiratory effects
1. bronchial constriction
2. narrowed airways
I At recommended doses, the cholinergics primarily affect the muscarinic receptors.
1. desired effect are from the stimulation of muscarinic
J. At high doses they stimulate the nicotinic receptors.
1. many undesirable effects are due to stimulation of nicotinic receptors.
***focus on drug effects for muscarinic...sludgeIV Indications
A. direct acting
1. reduce intraocular pressure
2. useful for glaucoma and intraocular surgery
a. acetylcholine, carbachol, pilocarpine
3. topical application due to poor oral absorption
4. bethanechol
a. increases tone and motility of bladder and GI tract
b.
Chapter 19
I Cholinergic Agents: drugs that stimulate the PSNS (parasympathetic nervous system). The opposing system to the SNS. (seemed to be used in biological warfare)
A. Rest or digest.
B. only one we need to know is ACh.
C. AKA as cholinergic agonists or parasympathomimetics.
D. Mimic the effects of the PSNS neurotransmitter acetylcholine (ACh)
E. 2 types determined by location and action once stimulated
1. Nicotinic receptors
a. Located in the ganglia of both the PSNS and SNS
b. Named “nicotinic” bc can be stimulated by the alkaloid nicotine
2. Muscarinic receptors
a. Located postsynaptically
1. smooth muscle
2. cardiac muscle
3. glands of parasympathetic fibers
4. effector organs of cholinergic sympathetic fibers
b. Can be stimulated by the alkaloid muscarine
II Mechanism of Action
A. Direct acting cholinergic agonists
1. bind to cholinergic receptors, activating them
B. Indirect acting (cholinesterase inhibitors)
1. inhibit the enzyme cholinesterase which breaks down ACh
2. result: more ACh is available at the receptors
3. can be:
a. reversible: bind to cholinesterase for a period of minutes or hours
b. irreversible: bind to cholinesterase and form a permanent covalent bond. The body must make new cholinesterase as in nerve gas damage.
III Drug Effects
A. Effects seen when the PSNS is stimulated
B. The PSNS is the “rest and digest” system
C. SLUDGE (some kind of excretion)
Salivation
Lacrimation (tears)
Urinary incontinence
Diarrhea
Gastrointestinal cramps
Emesis
D. Stimulate intestine and bladder
1. increased gastric secretions
2. increased GI motility
3. increased urinary frequency
E. stimulate pupil
1. contriction (miosis)
2. reduced intraocular pressure (used for glaucoma)
F. increased salivation and sweating
G. Cardiovascular effects
1. decreased heart rate
2. vasoldilation
H. respiratory effects
1. bronchial constriction
2. narrowed airways
I At recommended doses, the cholinergics primarily affect the muscarinic receptors.
1. desired effect are from the stimulation of muscarinic
J. At high doses they stimulate the nicotinic receptors.
1. many undesirable effects are due to stimulation of nicotinic receptors.
***focus on drug effects for muscarinic...sludgeIV Indications
A. direct acting
1. reduce intraocular pressure
2. useful for glaucoma and intraocular surgery
a. acetylcholine, carbachol, pilocarpine
3. topical application due to poor oral absorption
4. bethanechol
a. increases tone and motility of bladder and GI tract
b.
Cholinergic Agents
Cholinergic Agents
Chapter 19
I Cholinergic Agents: drugs that stimulate the PSNS (parasympathetic nervous system). The opposing system to the SNS. (seemed to be used in biological warfare)
A. Rest or digest.
B. only one we need to know is ACh.
C. AKA as cholinergic agonists or parasympathomimetics.
D. Mimic the effects of the PSNS neurotransmitter acetylcholine (ACh)
E. 2 types determined by location and action once stimulated
1. Nicotinic receptors
a. Located in the ganglia of both the PSNS and SNS
b. Named “nicotinic” bc can be stimulated by the alkaloid nicotine
2. Muscarinic receptors
a. Located postsynaptically
1. smooth muscle
2. cardiac muscle
3. glands of parasympathetic fibers
4. effector organs of cholinergic sympathetic fibers
b. Can be stimulated by the alkaloid muscarine
II Mechanism of Action
A. Direct acting cholinergic agonists
1. bind to cholinergic receptors, activating them
B. Indirect acting (cholinesterase inhibitors)
1. inhibit the enzyme cholinesterase which breaks down ACh
2. result: more ACh is available at the receptors
3. can be:
a. reversible: bind to cholinesterase for a period of minutes or hours
b. irreversible: bind to cholinesterase and form a permanent covalent bond. The body must make new cholinesterase as in nerve gas damage.
III Drug Effects
A. Effects seen when the PSNS is stimulated
B. The PSNS is the “rest and digest” system
C. SLUDGE (some kind of excretion)
Salivation
Lacrimation (tears)
Urinary incontinence
Diarrhea
Gastrointestinal cramps
Emesis
D. Stimulate intestine and bladder
1. increased gastric secretions
2. increased GI motility
3. increased urinary frequency
E. stimulate pupil
1. contriction (miosis)
2. reduced intraocular pressure (used for glaucoma)
F. increased salivation and sweating
G. Cardiovascular effects
1. decreased heart rate
2. vasoldilation
H. respiratory effects
1. bronchial constriction
2. narrowed airways
I At recommended doses, the cholinergics primarily affect the muscarinic receptors.
1. desired effect are from the stimulation of muscarinic
J. At high doses they stimulate the nicotinic receptors.
1. many undesirable effects are due to stimulation of nicotinic receptors.
***focus on drug effects for muscarinic...sludgeIV Indications
A. direct acting
1. reduce intraocular pressure
2. useful for glaucoma and intraocular surgery
a. acetylcholine, carbachol, pilocarpine
3. topical application due to poor oral absorption
4. bethanechol
a. increases tone and motility of bladder and GI tract
b.
Chapter 19
I Cholinergic Agents: drugs that stimulate the PSNS (parasympathetic nervous system). The opposing system to the SNS. (seemed to be used in biological warfare)
A. Rest or digest.
B. only one we need to know is ACh.
C. AKA as cholinergic agonists or parasympathomimetics.
D. Mimic the effects of the PSNS neurotransmitter acetylcholine (ACh)
E. 2 types determined by location and action once stimulated
1. Nicotinic receptors
a. Located in the ganglia of both the PSNS and SNS
b. Named “nicotinic” bc can be stimulated by the alkaloid nicotine
2. Muscarinic receptors
a. Located postsynaptically
1. smooth muscle
2. cardiac muscle
3. glands of parasympathetic fibers
4. effector organs of cholinergic sympathetic fibers
b. Can be stimulated by the alkaloid muscarine
II Mechanism of Action
A. Direct acting cholinergic agonists
1. bind to cholinergic receptors, activating them
B. Indirect acting (cholinesterase inhibitors)
1. inhibit the enzyme cholinesterase which breaks down ACh
2. result: more ACh is available at the receptors
3. can be:
a. reversible: bind to cholinesterase for a period of minutes or hours
b. irreversible: bind to cholinesterase and form a permanent covalent bond. The body must make new cholinesterase as in nerve gas damage.
III Drug Effects
A. Effects seen when the PSNS is stimulated
B. The PSNS is the “rest and digest” system
C. SLUDGE (some kind of excretion)
Salivation
Lacrimation (tears)
Urinary incontinence
Diarrhea
Gastrointestinal cramps
Emesis
D. Stimulate intestine and bladder
1. increased gastric secretions
2. increased GI motility
3. increased urinary frequency
E. stimulate pupil
1. contriction (miosis)
2. reduced intraocular pressure (used for glaucoma)
F. increased salivation and sweating
G. Cardiovascular effects
1. decreased heart rate
2. vasoldilation
H. respiratory effects
1. bronchial constriction
2. narrowed airways
I At recommended doses, the cholinergics primarily affect the muscarinic receptors.
1. desired effect are from the stimulation of muscarinic
J. At high doses they stimulate the nicotinic receptors.
1. many undesirable effects are due to stimulation of nicotinic receptors.
***focus on drug effects for muscarinic...sludgeIV Indications
A. direct acting
1. reduce intraocular pressure
2. useful for glaucoma and intraocular surgery
a. acetylcholine, carbachol, pilocarpine
3. topical application due to poor oral absorption
4. bethanechol
a. increases tone and motility of bladder and GI tract
b.
More Adrenergic Drugs
Adrenergic Drugs
Chapter 17 Outline
I Adrenergic Drugs
A. Drugs with effects that are similar to or mimic the effects of the SNS neurotransmitters NE, EPI, and dopamine.
B. Catecholamine: produces a sympathomimetic response.
1. endogenous
a. NE: stimulate Alpha
b. Epi: stimulates Beta
c. dopamine: dopaminergic receptors
2. synthetic
a. dobutamine
b. phenylephrine
c. isoproterenol
C. When these drugs are given they bathe the area between the nerve and the effector cell (synaptic cleft) and induces a response. (agonist b/c they bind to receptors and cause a response)
1. direct: binds to a receptor and causes a physiologic response. Drug itself binds to receptor.
a. EPI
b. NE
2. indirect: causes release of catecholamines from the storage sites (vesicles) in the nerve endings. Drug releases endongenous catech.
a. amphetamine
3. combination: directly stimulates the receptor by binding to it and indirectly stimulates the receptor by causing the release of the neurotrans stored in the vesicles at the nerve endings
a. ephedrine
II Noncatecholamine adrenergic drugs: structurally dissimilar to the endogenous catecholamines and generally have a longer duration of action than either the endogenous or synthetic catecholamines.
A. Phenylephrine
B. metaproterenol
C. albuterol
III Mechanism of Action and Drug Effects
A. When the drugs stimulate Alpha 1 smooth muscle, vasoconstriction occurs
1. blood vessels: vasoconstriction
2. CNS stimulation (speed, amphetamine)
2. GI smooth muscles: relaxation
3. Uterus and bladder: contraction
4. male ejaculation
5. decreased insulin release
6. contraction of the ciliary muscles resulting in dilation, mydriasis
B. Beta 1: myocardium & conduction of heart
1. increased force of contraction (Positive Inotropic Effect)
2. increase in heart rate (positive chronotropic effect)
3. increase in nerve impulses AVnode (positive dromotropic effect)
C. Beta 2:
1. relaxation of the bronchi (bronchodilation)
2. relaxation of the uterus
3. increased glycogenolysis in the liver
4. increase in renin secretion in the kidneys
IV Indications
A. Respiratory
1. bronchodilators: B2 (may also affect uterine and vascular smooth muscles)
a. asthma
b. bronchitis
c. albuterol, bitolterol, ephedrine, epinephrine, formoterol, salmeterol,
B. Topical Nasal Decongestants
1. A1: constriction of dilated arterioles & reduction in nasal blood flow decreasing congestion
a. epi, ephedrine, naphazoline, phenylephrine, tetrahydrozoline
C. Opthalmic
1. A1
2. temporarily relieve conjunctival congestion by causing arteriolar vasoconstriction.
a. epinephrine, phenylephrine, naphazoline, tetrahydrozoline (Visine)
3. reduce intraocular pressure and dilate the pupils (mydriasis) helpful in glaucoma. Stimulate A1 or B2 or both.
a. epinephrine
b. dipivefrin
D. Cardiovascular
1. AKA: cardioselective/vasoactive sympathomimetics, vasoconstrictive drugs, vasopressive, pressors, inotropes
2. Used to support the heart during cardiac failure or shock.
3. Variety of effects on various Alpha and Beta receptors which are related to the specific dose of the drug.
4. dobutamine (a, b), dopamine (a, b, dopa), epinephrine (a + b), norepinephrine (a + b)
5. In practice we use what works best. Can run meds together.
a. epi: increase heart rate
b. ne: constrict blood vessels (raise bp, lower pulse)
c. dopamine: from chart
d. dobutamine: heart beat stronger
V About the Receptors: (see chart for organs affected)
A. Alpha
1. located on presynaptic nerve terminals
2. control the release of neurotransmitters
3. alpha-adrenergic agonist responses
a. vasoconstriction
b. CNS stimulation (speed)
B. Beta
1. located on postsynaptic effector cells (organ itself)
2. Beta 1 = heart
3. Beta 2 = lungs (smooth muscle of the bronchioles, arterioles, and visceral organs)
C. Dopaminergic receptors
1. an additional adrenergic receptor
2. stimulated by dopamine
3. Causes dilation resulting in increased blood flow of:
a. renal
b. mesenteric
c. coronary
d. cerebral
VI Contradictions
A. Only known allergy and severe hypertension
VII Adverse Effects (many are the same for alpha and beta)
A. Alpha
1. CNS effects
a. headache
b. restlessness
c. excitement
d. insomnia
e. euphoria
2. cardiovascular
a. chest pain
b. vasoconstriction
c. hypertension
d. tachycardia
e. palpitations
f. dysrhythmias
3. other systems
a. anorexia
b. dry mouth
c. nausea
d. vomiting
e. taste changes (rarely)
B. Beta
1. CNS
a. mild tremors
b. headache
c. nervousness
d. dizziness
2. cardiovascular
a. increased heart rate
b. palpitations (dysrhythmias)
c. fluctuations in BP
3. other systems
a. sweating
b. nausea
c. vomiting
d. muscle cramps
VIII Interactions
A. Anesthetic agents
B. tricyclic antidepressants
C. MAOI’s
D. Antihistamines
E. thyroid preparations
F. antihypertensives
G. Will directly antagonize another adrenergic agent, resulting in reduced effects. We never usually use 2 at once.
Nursing Implications
I Assess
A. for allergies
B. history of HPN
C. cardiac dysrhythmias
D. other cardiovascular disease
E. renal, hepatic, and cardiac function before treatment.
II Perform baseline assessment of vital signs, peripheral pulses, skin color, temperature, and capillary refill. Include postural bp and pulse
III follow administration guidelines
IV IV administration
A. check iv site often for infiltration
B. use clear iv solutions
C. use an infusion device/IV pump
D. infuse agent slowly/properly to avoid dangerous CV effects
E. monitor cardiac rhythm
V In chronic lung disease
A. instruct pts to avoid factors that exacerbate their condition
B. encourage fluid intake (up to 3000ml/day if permitted)
C. educate about proper dosing, use of equipment (MDI, spacer, nebulizer) and equipment care.
Etc:
Salmeterol is indicated for prevention of bronchospasms, not management of acute symptoms.
Overuse of nasal decongestants may cause rebound nasal congestion or ulcerations.
Avoid OTC or other medications b/c of possible interactions.
Administering 2 adrenergic agents together may precipitate severe cardiovascular effects such as tachycardia or HPN.
Inform pts taking inhaled isoproterenol that their sputum may turn pink.
Monitor for therapeutic effects:
A. cardiovascular:
1. decreased edema
2. increased urinary output
3. return to normal vital signs
4. improved skin color and temp
5. increase LOC
B. asthma
1. return to normal respiratory rate
2. improved breath sounds, fewer rales
3. increased air exchange
4. decreased cough
5. less dyspnea
6. improved blood gasses
7. increased activity tolerance
If the heart is damaged or in failure give vasoactive sympathomimetics (pressors) b/c it makes the heart beat harder/faster. Helps support heart during cardiac failure or shock. (When in shock blood vessels dilate)
This chapter made simple:
NE: constricts blood vessels
Epi: increases heart rate...used in shock
Dopa: increases blood flow to kidneys
Dobutamine: heart to beat strong/fast
Questions
Which of the following are naturally occurring and can also be synthesized? (NE, epi, dopamine)
Which of the following causes an increased force of contraction? (inotropic, chromotropic, dromotropic)
Can we give epi pen for an asthma attack?
Constricts blood vessels
Increases heart rate
Increases conduct
Dilates lungs
Yes, b/c asthma constricts the lungs, epi dilates. The problem is the side effect of raising the heart rate.
Can we use albuterol for a b sting? (no effect on alpha 1)
Will epi cause beta 2 effects?
When we think of adrenergic basic concept we are talking about 3 receptors: Alpha, beta, dopa.
When we speak of adernergic/ sympathomimetic system we know A1 is our primary receptor that causes vaso constriction overall. B1, heart. B2, lungs.
Dopa receptors are: kidney, coronary, cerebral, messentary and they have the opposite effect where dilation INCREASES blood flow.
Primary drugs are NE, EPI, and albuterol
NE and epi affect both alpha1, and both betas. Dopa affects only dopaminergic receptors.
Chapter 17 Outline
I Adrenergic Drugs
A. Drugs with effects that are similar to or mimic the effects of the SNS neurotransmitters NE, EPI, and dopamine.
B. Catecholamine: produces a sympathomimetic response.
1. endogenous
a. NE: stimulate Alpha
b. Epi: stimulates Beta
c. dopamine: dopaminergic receptors
2. synthetic
a. dobutamine
b. phenylephrine
c. isoproterenol
C. When these drugs are given they bathe the area between the nerve and the effector cell (synaptic cleft) and induces a response. (agonist b/c they bind to receptors and cause a response)
1. direct: binds to a receptor and causes a physiologic response. Drug itself binds to receptor.
a. EPI
b. NE
2. indirect: causes release of catecholamines from the storage sites (vesicles) in the nerve endings. Drug releases endongenous catech.
a. amphetamine
3. combination: directly stimulates the receptor by binding to it and indirectly stimulates the receptor by causing the release of the neurotrans stored in the vesicles at the nerve endings
a. ephedrine
II Noncatecholamine adrenergic drugs: structurally dissimilar to the endogenous catecholamines and generally have a longer duration of action than either the endogenous or synthetic catecholamines.
A. Phenylephrine
B. metaproterenol
C. albuterol
III Mechanism of Action and Drug Effects
A. When the drugs stimulate Alpha 1 smooth muscle, vasoconstriction occurs
1. blood vessels: vasoconstriction
2. CNS stimulation (speed, amphetamine)
2. GI smooth muscles: relaxation
3. Uterus and bladder: contraction
4. male ejaculation
5. decreased insulin release
6. contraction of the ciliary muscles resulting in dilation, mydriasis
B. Beta 1: myocardium & conduction of heart
1. increased force of contraction (Positive Inotropic Effect)
2. increase in heart rate (positive chronotropic effect)
3. increase in nerve impulses AVnode (positive dromotropic effect)
C. Beta 2:
1. relaxation of the bronchi (bronchodilation)
2. relaxation of the uterus
3. increased glycogenolysis in the liver
4. increase in renin secretion in the kidneys
IV Indications
A. Respiratory
1. bronchodilators: B2 (may also affect uterine and vascular smooth muscles)
a. asthma
b. bronchitis
c. albuterol, bitolterol, ephedrine, epinephrine, formoterol, salmeterol,
B. Topical Nasal Decongestants
1. A1: constriction of dilated arterioles & reduction in nasal blood flow decreasing congestion
a. epi, ephedrine, naphazoline, phenylephrine, tetrahydrozoline
C. Opthalmic
1. A1
2. temporarily relieve conjunctival congestion by causing arteriolar vasoconstriction.
a. epinephrine, phenylephrine, naphazoline, tetrahydrozoline (Visine)
3. reduce intraocular pressure and dilate the pupils (mydriasis) helpful in glaucoma. Stimulate A1 or B2 or both.
a. epinephrine
b. dipivefrin
D. Cardiovascular
1. AKA: cardioselective/vasoactive sympathomimetics, vasoconstrictive drugs, vasopressive, pressors, inotropes
2. Used to support the heart during cardiac failure or shock.
3. Variety of effects on various Alpha and Beta receptors which are related to the specific dose of the drug.
4. dobutamine (a, b), dopamine (a, b, dopa), epinephrine (a + b), norepinephrine (a + b)
5. In practice we use what works best. Can run meds together.
a. epi: increase heart rate
b. ne: constrict blood vessels (raise bp, lower pulse)
c. dopamine: from chart
d. dobutamine: heart beat stronger
V About the Receptors: (see chart for organs affected)
A. Alpha
1. located on presynaptic nerve terminals
2. control the release of neurotransmitters
3. alpha-adrenergic agonist responses
a. vasoconstriction
b. CNS stimulation (speed)
B. Beta
1. located on postsynaptic effector cells (organ itself)
2. Beta 1 = heart
3. Beta 2 = lungs (smooth muscle of the bronchioles, arterioles, and visceral organs)
C. Dopaminergic receptors
1. an additional adrenergic receptor
2. stimulated by dopamine
3. Causes dilation resulting in increased blood flow of:
a. renal
b. mesenteric
c. coronary
d. cerebral
VI Contradictions
A. Only known allergy and severe hypertension
VII Adverse Effects (many are the same for alpha and beta)
A. Alpha
1. CNS effects
a. headache
b. restlessness
c. excitement
d. insomnia
e. euphoria
2. cardiovascular
a. chest pain
b. vasoconstriction
c. hypertension
d. tachycardia
e. palpitations
f. dysrhythmias
3. other systems
a. anorexia
b. dry mouth
c. nausea
d. vomiting
e. taste changes (rarely)
B. Beta
1. CNS
a. mild tremors
b. headache
c. nervousness
d. dizziness
2. cardiovascular
a. increased heart rate
b. palpitations (dysrhythmias)
c. fluctuations in BP
3. other systems
a. sweating
b. nausea
c. vomiting
d. muscle cramps
VIII Interactions
A. Anesthetic agents
B. tricyclic antidepressants
C. MAOI’s
D. Antihistamines
E. thyroid preparations
F. antihypertensives
G. Will directly antagonize another adrenergic agent, resulting in reduced effects. We never usually use 2 at once.
Nursing Implications
I Assess
A. for allergies
B. history of HPN
C. cardiac dysrhythmias
D. other cardiovascular disease
E. renal, hepatic, and cardiac function before treatment.
II Perform baseline assessment of vital signs, peripheral pulses, skin color, temperature, and capillary refill. Include postural bp and pulse
III follow administration guidelines
IV IV administration
A. check iv site often for infiltration
B. use clear iv solutions
C. use an infusion device/IV pump
D. infuse agent slowly/properly to avoid dangerous CV effects
E. monitor cardiac rhythm
V In chronic lung disease
A. instruct pts to avoid factors that exacerbate their condition
B. encourage fluid intake (up to 3000ml/day if permitted)
C. educate about proper dosing, use of equipment (MDI, spacer, nebulizer) and equipment care.
Etc:
Salmeterol is indicated for prevention of bronchospasms, not management of acute symptoms.
Overuse of nasal decongestants may cause rebound nasal congestion or ulcerations.
Avoid OTC or other medications b/c of possible interactions.
Administering 2 adrenergic agents together may precipitate severe cardiovascular effects such as tachycardia or HPN.
Inform pts taking inhaled isoproterenol that their sputum may turn pink.
Monitor for therapeutic effects:
A. cardiovascular:
1. decreased edema
2. increased urinary output
3. return to normal vital signs
4. improved skin color and temp
5. increase LOC
B. asthma
1. return to normal respiratory rate
2. improved breath sounds, fewer rales
3. increased air exchange
4. decreased cough
5. less dyspnea
6. improved blood gasses
7. increased activity tolerance
If the heart is damaged or in failure give vasoactive sympathomimetics (pressors) b/c it makes the heart beat harder/faster. Helps support heart during cardiac failure or shock. (When in shock blood vessels dilate)
This chapter made simple:
NE: constricts blood vessels
Epi: increases heart rate...used in shock
Dopa: increases blood flow to kidneys
Dobutamine: heart to beat strong/fast
Questions
Which of the following are naturally occurring and can also be synthesized? (NE, epi, dopamine)
Which of the following causes an increased force of contraction? (inotropic, chromotropic, dromotropic)
Can we give epi pen for an asthma attack?
Constricts blood vessels
Increases heart rate
Increases conduct
Dilates lungs
Yes, b/c asthma constricts the lungs, epi dilates. The problem is the side effect of raising the heart rate.
Can we use albuterol for a b sting? (no effect on alpha 1)
Will epi cause beta 2 effects?
When we think of adrenergic basic concept we are talking about 3 receptors: Alpha, beta, dopa.
When we speak of adernergic/ sympathomimetic system we know A1 is our primary receptor that causes vaso constriction overall. B1, heart. B2, lungs.
Dopa receptors are: kidney, coronary, cerebral, messentary and they have the opposite effect where dilation INCREASES blood flow.
Primary drugs are NE, EPI, and albuterol
NE and epi affect both alpha1, and both betas. Dopa affects only dopaminergic receptors.
Adrenergic Blocking Drugs
Adrenergic Blocking Drugs
Chapter 18
I Adrenergic blocking
A. opposite effect of agonist adrenergic drugs.
B. antagonists: bind to receptors and inhibit/block stimulation by the SNS.
C. AKA sympatholytics because they lyse/inhibit SNS stimulation.
II Alpha blockers
A. block a1 and a2 receptors
B. effects:
1. both arterial and venous dilation reducing peripheral vascular resistance and bp
2. used to treat HPN
3. on prostate gland and bladder decreased resistance to urinary outflow, thus reducing urinary obstruction and relieving effects of BPH (benign prostatic hyperplasia)
4. used to control and prevent hypertension in pts with pheochromocytoma
5. phentolamine is a blocker that (counteracts):
a. quickly reverses the potent vasoconstrictive effects of extravasated vasopressors such as norepinephrine or epinephrine.
(infiltrated vasopressors will stop blood flow and kill tissues)
b. restores blood flow and prevents tissue necrosis (death)
C. side effects:
1. cardiovascular:
a. palpitations
b. orthostatic hypotension
c. tachycardia
d. edema
e. dysrhythmias
f. chest pain
2. CNS
a. dizziness
b. headache
c. drowsiness
d. anxiety
e. vertigo
f. weakness
g. numbness
h. fatigue
3. gastrointestinal
a. nausea
b. vomiting
c. diarrhea
d. constipation
e. abdominal pain
4. other
a. incontinence
b. nosebleed
c. tinnitus
d. dry mouth
e. pharyngitis
f. rhinitis
D. Common agents
1. phentolamine (regitine)
2. prazosin (minipress)
3. tolazoline (priscoline)
E. Contraindications
1. known drug allergy
2. peripheral vascular disease
3. may include: hepatic and renal disease, CAD, peptic ulcer, sepsis
III Beta Blockers
A. block stimulation of beta 1 & 2 receptors in the SNS
B. compete with norepinephrine and epineprhine
C. 2 types
1. selective aka cardioselective: Beta 1 blocker selective for those on receptors on the heart are called cardioselective
2. nonselective aka nonspecific blockers are effective on both b1 and b2 receptors
D. Mechanism of action
1. cardioselective (b1)
a. reduces SNS stimulation of the heart
b. decreases heart rate
c. prolongs SA node recovery
d. slows conduction rate through the AV node
e. decreases myocardial contractility, thus decreasing myocardial o2 demand.
***. a and b for b/p
b, c, d, for afib
a and d for heart failure(congestive), heart attack (post MI), and angina
2. nonspecific (b1 and b2)
a. effects on heart: same as cardioselective
b. effects on bronchioles: constriction resulting in narrowing of the airways and SOB
c. blood vessels: vasoconstriction
E. Indications
1. antiangina: decreases demand for myocardial o2
2. cardioprotective: inhibits stimulation from circulating catecholamines
3. class II antidysrhythmic
4. anthi HPN
5. treatment of migraine headaches
6. glaucoma (topical use)
F. Side effects
1. blood
a. agranulocytosis
b. thrombocytopenia (decreased platelets)
2. cardiovascular
a. av block
b. bradycardia
c. heart failure
d. peripheral vascular insufficiency
3. CNS
a. dizziness
b. mental depression
c. lethargy
d. hallucinations
e. impotence
4. gastrointestinal
a. nausea
b. dry mouth
c. vomiting
d. diarrhea
e. cramps
f. ischemic colitis
5. other
a. impotence
b. rash
c. alopecia
d. bronchospasm
G. Common agents
1. atenolol (tenormin) selective
2. carvedilol (coreg) selective beta, & alpha
3. labetalol (trandate) same as above
4. sotalol (betapace)
5. metoprolol (lopressor) selective
6. propranolol (inderol) nonselective
7. Newer beta blockers with once a day dosing:
a. betazolol
b. besoprolol
Nursing Implications
I Assess
A. allergies
B. history of COPD
C. hypotension
D. cardiac dysrhythmias
E. bradycardia, HF, or other CV problems
F. any preexisting condition that might be exacerbated by the use of these agents might be a contraindication to their use.
Alpha blockers may precipitate hypotension.
Some beta blockers may precipitate bradycardia, hypotension, heart block, HF and bronchoconstriction.
Avoid OTC meds bc of possible interactions.
Possible drug interactions may occur with:
Anacids (aluminum hydroxide type)
Antimuscarinics/anticholinergics
Diuretics and cardiovascular drugs
Neuromuscular blocking agents
Oral hypoglycemic agents
Encourage patients to take meds as prescribed.
These meds should never be stopped abruptly.
Report constipation or the development of any urinary hesitancy or bladder distension.
Teach pts to change positions slowly to prevent or minimize postural hypotension.
Avoid caffeine (excessive irritability)
Avoid alcohol ingestion and hazardous activities until blood levels become stable.
Pts should notify their physician if palpitations, dyspnea, nausea, or vomiting occur.
Monitor side effects.
Therapeutic effects: decreased angina, return to normal bp and pulse, etc.
ETC...
Beta blocker DO NOT vasodilate. They have no effect on Alpha. They decrease peripheral vascular resistance. Blocks responses of neurotransmitters on beta receptors.
What are the mechanisms of action for BP? A and b.
What are the mechanisms of action of beta blocker for treatment of afib? 2+3+4
“ .....” for CHF 1 + 5
Or heart attack “”.
The mechanism of action in a beta blocker in heart failure is which of the following?
(pay attention! May be more than one answer)
True or false....
Nonselective beta blockers should not be used in asthma pts. (true)
Alpha blockers should never be used in asthma pts. false
Beta blockers work on CHF bc the heart wants to beat faster bc it is “broke”. NE makes it beat faster, but we need rest to heal. Give a beta blocker to allow rest.
Chapter 18
I Adrenergic blocking
A. opposite effect of agonist adrenergic drugs.
B. antagonists: bind to receptors and inhibit/block stimulation by the SNS.
C. AKA sympatholytics because they lyse/inhibit SNS stimulation.
II Alpha blockers
A. block a1 and a2 receptors
B. effects:
1. both arterial and venous dilation reducing peripheral vascular resistance and bp
2. used to treat HPN
3. on prostate gland and bladder decreased resistance to urinary outflow, thus reducing urinary obstruction and relieving effects of BPH (benign prostatic hyperplasia)
4. used to control and prevent hypertension in pts with pheochromocytoma
5. phentolamine is a blocker that (counteracts):
a. quickly reverses the potent vasoconstrictive effects of extravasated vasopressors such as norepinephrine or epinephrine.
(infiltrated vasopressors will stop blood flow and kill tissues)
b. restores blood flow and prevents tissue necrosis (death)
C. side effects:
1. cardiovascular:
a. palpitations
b. orthostatic hypotension
c. tachycardia
d. edema
e. dysrhythmias
f. chest pain
2. CNS
a. dizziness
b. headache
c. drowsiness
d. anxiety
e. vertigo
f. weakness
g. numbness
h. fatigue
3. gastrointestinal
a. nausea
b. vomiting
c. diarrhea
d. constipation
e. abdominal pain
4. other
a. incontinence
b. nosebleed
c. tinnitus
d. dry mouth
e. pharyngitis
f. rhinitis
D. Common agents
1. phentolamine (regitine)
2. prazosin (minipress)
3. tolazoline (priscoline)
E. Contraindications
1. known drug allergy
2. peripheral vascular disease
3. may include: hepatic and renal disease, CAD, peptic ulcer, sepsis
III Beta Blockers
A. block stimulation of beta 1 & 2 receptors in the SNS
B. compete with norepinephrine and epineprhine
C. 2 types
1. selective aka cardioselective: Beta 1 blocker selective for those on receptors on the heart are called cardioselective
2. nonselective aka nonspecific blockers are effective on both b1 and b2 receptors
D. Mechanism of action
1. cardioselective (b1)
a. reduces SNS stimulation of the heart
b. decreases heart rate
c. prolongs SA node recovery
d. slows conduction rate through the AV node
e. decreases myocardial contractility, thus decreasing myocardial o2 demand.
***. a and b for b/p
b, c, d, for afib
a and d for heart failure(congestive), heart attack (post MI), and angina
2. nonspecific (b1 and b2)
a. effects on heart: same as cardioselective
b. effects on bronchioles: constriction resulting in narrowing of the airways and SOB
c. blood vessels: vasoconstriction
E. Indications
1. antiangina: decreases demand for myocardial o2
2. cardioprotective: inhibits stimulation from circulating catecholamines
3. class II antidysrhythmic
4. anthi HPN
5. treatment of migraine headaches
6. glaucoma (topical use)
F. Side effects
1. blood
a. agranulocytosis
b. thrombocytopenia (decreased platelets)
2. cardiovascular
a. av block
b. bradycardia
c. heart failure
d. peripheral vascular insufficiency
3. CNS
a. dizziness
b. mental depression
c. lethargy
d. hallucinations
e. impotence
4. gastrointestinal
a. nausea
b. dry mouth
c. vomiting
d. diarrhea
e. cramps
f. ischemic colitis
5. other
a. impotence
b. rash
c. alopecia
d. bronchospasm
G. Common agents
1. atenolol (tenormin) selective
2. carvedilol (coreg) selective beta, & alpha
3. labetalol (trandate) same as above
4. sotalol (betapace)
5. metoprolol (lopressor) selective
6. propranolol (inderol) nonselective
7. Newer beta blockers with once a day dosing:
a. betazolol
b. besoprolol
Nursing Implications
I Assess
A. allergies
B. history of COPD
C. hypotension
D. cardiac dysrhythmias
E. bradycardia, HF, or other CV problems
F. any preexisting condition that might be exacerbated by the use of these agents might be a contraindication to their use.
Alpha blockers may precipitate hypotension.
Some beta blockers may precipitate bradycardia, hypotension, heart block, HF and bronchoconstriction.
Avoid OTC meds bc of possible interactions.
Possible drug interactions may occur with:
Anacids (aluminum hydroxide type)
Antimuscarinics/anticholinergics
Diuretics and cardiovascular drugs
Neuromuscular blocking agents
Oral hypoglycemic agents
Encourage patients to take meds as prescribed.
These meds should never be stopped abruptly.
Report constipation or the development of any urinary hesitancy or bladder distension.
Teach pts to change positions slowly to prevent or minimize postural hypotension.
Avoid caffeine (excessive irritability)
Avoid alcohol ingestion and hazardous activities until blood levels become stable.
Pts should notify their physician if palpitations, dyspnea, nausea, or vomiting occur.
Monitor side effects.
Therapeutic effects: decreased angina, return to normal bp and pulse, etc.
ETC...
Beta blocker DO NOT vasodilate. They have no effect on Alpha. They decrease peripheral vascular resistance. Blocks responses of neurotransmitters on beta receptors.
What are the mechanisms of action for BP? A and b.
What are the mechanisms of action of beta blocker for treatment of afib? 2+3+4
“ .....” for CHF 1 + 5
Or heart attack “”.
The mechanism of action in a beta blocker in heart failure is which of the following?
(pay attention! May be more than one answer)
True or false....
Nonselective beta blockers should not be used in asthma pts. (true)
Alpha blockers should never be used in asthma pts. false
Beta blockers work on CHF bc the heart wants to beat faster bc it is “broke”. NE makes it beat faster, but we need rest to heal. Give a beta blocker to allow rest.
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