Nursing 308 > Blakely > Flashcards > Week Three - Lecture (No. 2 - no class last week)

Bactericidal vs. bacteriostatic

Bactericidal: kills bacteria
Bacteriostatic: prevents bacteria from multiplying/growing; may affect metabolism or another process

What is the goal of antibacterial therapy?

Kill bacteria or prevent their reproduction w/o harming the pt

What is in the cell wall of bacteria?

Endotoxins
Arachnoid acid
*Makes pts fever go up; more aches and pains with inflammatory cascade when meds start killing off bacteria*

What happens in pts who take drugs that destroy a bacteria's cell wall?

Makes pts fever go up; more aches and pains with inflammatory cascade when meds start killing off bacteria. This happens when endotoxins are released from the cell wall and arachnoid acid starts the inflammatory cascade.

What do the pregnancy categories on drugs mean?

A - the safest drug
C - research is suspicious; admin may cause problems
X - the worst; no one who is pregnant/breastfeeding should take this drug

Pharmacodynamics:

What the drugs do to the body. AKA biotransformation

How does the body change the drug?

- Changes the drug in some way
- Size
- Lipid solubility to water soluble
- Charge or polarity changes
- Activate or inactivate

Metabolism means:

Drug is being inactivated
Increased metabolism = more inactive, less bioavailable

No. 1 place for biotransformation is:

The liver
- intestines
- kidneys
- brain
- plasma

What happens if a pt has liver failure?

Lower dose and frequency b/c not metabolized

How does age affect biotransformation?

- infants: less enzymes; BBB less developed (leads to toxicity)
- elderly: less GI absorption; less renal clearance

Cytochrome P450 does what?

Metabolizes 50 to 70% of drugs
Many factors alter its effectiveness

Selectivity:

degree to drug does produces desired effect vs. adverse effects
dependent on specificity of drug

Specificity:

degree to which drug binds to single receptor type
IE: a drug for liver cancer

Agonist:

Drug that produces an effect comparable to endogenous ligand
IE: a drug that binds to a receptor and has an effect on the cell

Agonist I

bind to the same receptor site as endogenous ligand
direct effect
Ex: morphine

Agonist II:

bind to different receptor site than endogenous ligand
enhance receptor activity
indirect effect
Ex: Valium

Antagonist:

drug that inhibits the action of endogenous ligand by blocking the receptor

Antagonist I

competitive; compete for same binding site

Antagonist II

bind to a nearby site of endogenous ligand
Ex: digoxin

The main PNS neurotransmitter is:

acetylcholine

cholorgenic agents mimic PNS (anagonist)
anticholorgenic agents prohibit PNS (antagonist)

Symptomatic bradycardia med:

Give atropine IV;

given post-op to dry up secretions

Can a drug be an agonist and antagonist?

Yes

What is the combination of dose/time/effect?

Drug efficacy (Emax on chart): does at which max effect
Drug potency (ED50): dose at which get 50% of effect

Therapeutic Index (TI):

Ratio of drug concentration required to produce toxic effects compared to concentration to produce therapeutic response

What TI measurement do you want?

Greater than 1
Closer to 1, greater toxicity
Less than 1 = all toxic effects

How do you determine TI?

amt to produce toxic level/amt to be therapeutic = TI

Side effects vs. toxic effects

Side effects: action that occurs at therapeutic dose; annoying
Toxic effect: action that occurs when plasma blood concentration reaches toxic level, can be fatal

Geriatric considerations with med admin are:

- 65 yo+ are 13% pop & buy 35% of all prescription drugs
- body processes slow down
- slower metabolism
- impaired absorption
- decreased excretion

Predictable vs. unpredictable side effect

- Predictable
- Ex: antihistamines get drowsy
- Unpredictable
- Paradoxical: opposite effect
- Hypersensitivity: allergic rx
- Insensitive: no rx

If you have sedation, the drug must:

Cross the BBB

Polypharmacy:

use of multiple drugs to treat one or more health problems

What is a problem with polypharmacy?

Risk of drug-drug interaction increased with ea. additional drug taken
- Includes prescribed & OTC

The elderly typically take [blank] prescribed drugs/year.

11

Five drugs = 50% risk of adverse interactions
Eight drugs = 100% risk of adverse interactions

Do we know how drugs affect children?

No. They are typically not part of drug studies

What are ped considerations when admin drugs?

- Normal growth processes change the drug

How long does it take for a newborn, for a toddler to empty their stomach?

Newborn: 6-8 hours
Toddler: 2 hours

If you have more acid in your stomach, you will more readily absorb:

More acidic drugs; less absorb more alkaline drugs

How is the skin of a child different from an adult?

- Skin is thin
- Fewer layers
- Meds may be absorbed into the blood stream

What considerations do you need to have with IMs in children?

Less muscle mass, poorly developed peripheral circulation = decreased rate of absorption

How much fat do infants/toddlers/preschoolers have?

- Infants: 16%
- Toddlers: 23%
- Preschool: 8-12%

More fat = faster absorption of lipid soluble drugs

Children may have more biologically active drugs in blood b/c:

Less binding proteins in their body

Glomerular Filtration Rate (GFR) in kids is:

Half to 1/3 what adults have

Urine of a child is:

More acidic = increased re-absorption of acidic drugs

Hypersensitivity:

Exaggerated immune response

Anaphylaxis:

Systemic immune response that can result in death

Atopy:

Localized, predisposition to allergy

Allergy:

Localized immune response

The immune system protects against:

- Abnormal cells that have mutated
- Infectious pathogens

Normal immune response is:

- Phagocytosis
- Antigen show up
- Specific immune response
- Antibody mediated
- Cell-mediated
- Cytotoxic T-cells
- T-helper cells
- Th1: cell mediated
- Th2: antibody mediated

What is your first line of immune defense?

1) Skin
- IgA
- Enzymes
2) WBCs
- Neutrophils (phagocytosis)
- Macrophages (phagocytosis)

How does phagocytosis help develop antibodies?

They spit out part of the pathogen, which helps the B-cells develop antibodies

What is the function of T-cells?

- Activate B cells
- Kill the pathogen

Cytokines are released by:

T-cells.

What is the effect of cytokines?

They destroy the pathogen and enhance inflammation

What are the various types of WBCs?

- Granulocytes
- Neutrophils: phagocytosis
- Basophils (Mast cells): less than 1% ttl WBC count; 1/2 of body's histamine
- Eosinophils: function not known
- Lymphocytes
- B & T cells
- Natural killer cells: no immune response needed

Why are basophils (mast cells) important in the immune response?

has 1/2 of body's histamine; haywire = anaphylaxis

Ig means:

Antibody; it's made up of protein

Type I hypersensitivity:

- Rx can be local/systemic
- Local: atopy
- Systemic: anaphylaxis
- Must have:
- Prior exposure to allergen
- IgE
- Mast cell degranulation
- Anaphylaxis vs. Anaphylactoid rx

Anaphylaxis vs. Anaphylactoid rx

Anaphylactoid: no IgE; typically not as severe as anaphylaxis

What is the pathophysiology of Type I hypersensitivity?

IgE goes to mast cells; antigen hooks onto mast cell; when reinfected the IgE & mast cells go crazy; mast cell degranulates and releases histamine

What are the effects on the body of a Type I hypersensitivity?

Effects: smooth muscle contractions of bronchioles (bronchoconstriction), intestines (cramping), uterus (contraction-like pain), some vessels dilate (B/P drops)

Why is IgE produced in response to an allergen

- Genetic predisposition
- Th2: dominant response
- Ig E irreversibly binds to receptor on mast cells and basophils

Th2 dominate response means:

Ppl that normally fight off pathogens with antibodies

Increased antibody response = less cell-mediate response
And vice versa

Th2 dominate responders usually develop:

Allergies

What "mediators" are released FIRST by mast cells:

- Primary mediators
- Heparin
- Histamine
- Protease: break down vessels; lowers B/P; can lose 1/3 blood vol in 10 min. via third spacing
- Eosinophils & neutrophil chemotactic factors

What "mediated" factors are released in the next 24 hours by mast cells?

- Secondary mediators
- Leukotrines: drop B/P, leaking into tissues
- Prostaglandin GD2
- Platelet Activating Factor (PAF)
- Cytokines (IL -4; GM-CSF)

What are the clinical manifestation of anaphylaxis:

- Early phase: short-lived <1 hr.
- Vasodilation
- Capillary leaking
- Smooth muscle contration
- Microthrombi formation (in small vessels, no O2/nutrients)
- Gland hypersecretion: GI/skin (diaphoresis & diarrhea)
- Late phase
- inflammation: peaks at 5 hrs; last days
- Eosinophils, mast cells, basophils, T-cells an neutrophils, infiltration

Anaphylaxis tx:

- Rx cause removal
- Airway management
- Epinephrine
- alpha -1
- beta - 1
- beta - 2
- Drug tx
- inhaled beta-2 agonist
- anti-histamine
- corticosteroids
- fluids

What is epinephrine's effect on alpha-1 receptors?

Alpha- 1: vasoconstriction: raises B/P; heart beats stronger/faster

What is epinephrine's effect on beta-2 receptors?

Bronchodilation

Why do you give fluids in anaphylaxis?

Need circulating blood vol, despite third-spacing, for tissue perfusion

Why do you give corticosteroids?

Stabilize capillary leaking/membranes
Decrease inflammatory response

Atopy includes:

- Allergic rhinitis (nasal mucosa, conjunctiva)
- Asthma
- Food allergies
- Atopic dermatitis

Type I hypersensitivity tx:

- Allergy avoidance (allergy skin test)
- Stress avoidance
- Desensitization
- Drug tx
- Antihistamines
- Bronchodilators
- Allergy kit: benadryl + epinephrine
- Corticosteroids
- McAb
- IgE blocker binding

Stress tends to suppress:

Th1 cells = increased antibody response

Type II hypersensitivity mechanism:

- IgG & IgM
- antigen attaches to cell surface; immune activation; antibody released; tissue dmg/dysfunction

Tissue damage in Type II hypersensitivity is caused by:

- Opsonic adherence: phagocytosis
- Complement: membrane change
- Antibody dependence cell-mediated cytotoxicity (ADCC): cell destruction

How do antibodies destroy pathogens?

Like coating frosting on a brownie; attract WBCs to kill pathogen
Stimulate Th1 cells to come and do kiss of death

Normally phagocytic WBC are designed to attack:

One pathogen

In opsonic adherence phagocytic WBCs do what?

Various types swarm one pathogen and destroy it

Rh incompatibility:

Mother's immune cells attack the baby; (she is Rh-/baby is Rh+) the baby has no functioning RBCs and turn second Rh+ into a blue baby

Drug-induced hemolytic anemia:

RBC absorbs proteins; Anti-RBC IgG/IgM; complement, opsonization; ADCC; RBC lysis = anemia

Grave's disease etiology:

Antibodies (IgG & IgM) bind with TSH receptor on Thyroid Gland
Tell the thyroid to produce more thyroid hormone

Myasthenia Gravis etiology

Antibodies (IgG & IgM) to acetylcholine receptors on muscle cells
Need acetylcholine for muscle contraction
Effect = muscle weakness

Type III hypersensitivity mechanism:

- IgG & IgM
- Swim in body fluids (blood/lymphatic/joints)
- Antibodies attach to each other an antigens
- Make masses (embolism)
- Deposits in tissue: blood vessels, joints, kidneys

What would cause a Type III hypersensitivity rx:

Chronic, inflammatory reaction
Ex: MS; rheumatoid arthritis

What disease is a classic Type III hypersensitivity rx?

Systemic lupus erythematosis
Rheumatoid arthritis

s/s of Systemic Erythematosis

- butterfly rash across face
-

Type IV hypersensitivity mechanism is different b/c:

Only one that involves T cells

Type IV hypersensitivity mechanism:

- T-cell mediated
- 24-72 hrs after contact
- Stimulated by:
- Intracellular pathogens
- Contact with allergens
- Prolonged cell-mediated immunity

APC:

Antigen-presenting cell: a WBC

Type IV hypersensitivity develops at first exposure in:

One to two weeks

What happens in Type IV hypersensitivity after a second exposure?

- Onset 24 hr after exposure
- Peak 48-72 hours
- Th1 chemical mediators
- Macrophage activation
- Aggregation of Th2: lymphocytes & macrophages
- Granuloma

A broad spectrum of efficacy does not....

increase effectiveness
- Need C&S to know susceptible bacteria

What is the purpose of admin a cell wall synthesis inhibitor?

- Bactericidal
- Prevent bacteria from forming cell walls

What are the side effects of cell wall synthesis inhibitors?

- More likely to cause allergic rx
- With more powerful drugs - N&V, fever, chills, "red man syndrome," reduced hearing, reduced kidney function

Adverse effects of cell wall synthesis inhibitors?

CNS changes
kidney damage

Before admin cell wall synthesis inhibitors you should:

- Ck allergy to penicillin (increased risk for cephalosporin allergy)
- Give vancomycin slowly

After admin cell wall synthesis inhibitors you should:

- Monitor for allergic rx

What should you teach a pt about cell wall synthesis inhibitors?

- Take cephalosporins at least 1 hr before or 4 hrs after iron or antacid

How do children rx to cell wall synthesis inhibitors?

- More powerful drugs reserved for serious infections only

How do preggers/breastfeeding rx to cell wall synthesis inhibitors?

- Penicillins, most cephalosporins Class B
- Carbapenems, monobactams, vancomycin - Class C
- Excreted in breast milk

How do elderly rx to cell wall synthesis inhibitors?

- Ototoxicity, nephrotoxicity more likely

What is the common side effects of aminoglycosides?

N&V
Rash
Fever
Lethargy

What is the common side effects of macrolides?

N&V
Diarrhea
Loss of appetite
Photosensitivity

What is the common side effects of tetracyclines?

N&V
Diarrhea
Sore tongue
Photosensitivity
**Most likely to promote yeast infections**

What are the adverse effects of tetracyclines?

Increased intracranial pressure

What are the adverse effects of macrolides?

Many serious drug interactions

What are the adverse effects of aminoglycosides?

Ototoxicity, nephrotoxicity, neuromuscular blockade

What are the adverse effects of clindamycin?

Reduced liver function
DEC WBC counts

What are the adverse effects of Linezolid?

Reduced blood cell counts
Damage to optic nerve

What do you do before admin aminoglysides?

Assess breathing baseline, lab tests, hearing

What do you do before admin macrolides?

Ck other meds
Give IV erythromycin within 8 hrs of dilution

What do you do before admin tetracyclines?

Food, antacids and dairy DEC absorption

What do you check after admin animoglycosides?

Hearing
Temp
I&Os
Lab values (BUN & cratinine)

What do you check after admin macrolides?

HR & rhythm every 4 hours

What do you check after admin tetracyclines?

Warfarin: Ck for bleeding

What do you check after admin lizezolid?

BP

What do you teach a pt taking macrolides?

Take with food to DEC GI upset
Avoid the sun

What do you teach a pt taking tetracyclines?

Avoid the sun
Take an hour before meals or 2 hours after
Do NOT take with milk

What do you teach a pt taking linezolid?

Avoid taking with tyramine containing foods

How do children rx to aminoglycosides?

Cause severe respirator depression
Cause severe kidney damage

How do children rx to tetracyclines?

Should be avoided in children younger than 8

What protein synthesis inhibitor antibiotics are safe for preggers/breastfeeding?

Most macrolides are Class B
Most pass into breastmilk
Tetracyclines & Aminoglycosides: Class D

How do older adults respond to protein synthesis inhibitor antibiotics?

Ototoxicity
Nephrotoxicity

What are the two subtypes of metabolism inhibitor antibiotics?

Sulfonamides
Trimethoprim

How do metabolism inhibitor antibiotics work?

Bacteriostatic

Used to tx some non-bacterial infections: shigellosis, toxoplasmosis, etc.

What are common side effects for metabolism inhibitor antibiotics?

Headache
Fever
Skin rash
Photosensitivity

What are adverse effects of metabolism inhibitor antibiotics?

- Suppression of bone marrow division
- Steven-Johnson syndrome

What do you do before admin metabolism inhibitor antibiotics?

- Ck sulfa allergies
- Ck blood disorders
- Ck labs

What do you do AFTER admin metabolism inhibitor antibiotics?

- Ck jaundice, bruising, petechiae, blisters
- Offer water every 4 hours

What do you teach pts about metabolism inhibitor antibiotics?

- Avoid sun
- Take with a full glass of water
- Drink lots to prevent crystalluria

How do children rx to metabolism inhibitor antibiotics?

- Younger than 2 mos more likely to become jaundiced

How do preggers/breastfeeding rx to metabolism inhibitor antibiotics?

Class C
Avoid when breastfeeding
Avoid last 2 mos. of pregnancy

How do elderly rx to metabolism inhibitor antibiotics?

More intense side effects
Anemia
Increased bleeding risk

What drug class is a DNA synthesis inhibitor antibiotic?

Fluroquinolones

How do DNA synthesis inhibitor antibiotic work?

Inhibit production of DNA
Prevents bacterial reproduction

Side effects of DNA synthesis inhibitor antibiotic:

Rash
N&V
Headache
Abdominal pain
Dizziness
Change in taste

Adverse effects of DNA synthesis inhibitor antibiotic:

Serious heart dysrhythmias (esp when on other meds)
Neurotoxicity
Stevens-Johnson syndrome
Changes in blood glucose
Tendon rupture
Peripheral neuropathy

Before admin DNA synthesis inhibitor antibiotic:

- Ck if taking iron, vitamins or antacids
- Antidysrhythmic drug tx

AFTER admin DNA synthesis inhibitor antibiotic

- HR & rhythm every four hours

What do you teach a pt about DNA synthesis inhibitor antibiotic?

- Take with full glass of water
- Drink lots during day
- Check pulse bid
- Check blood glucose more often (diabetics)
- Tendon pain/swelling - stop drug and notify doc

How do children rx to fluoroquinolones?

- Not recommended <18 yo

How do preggers/breastfeeding rx to fluoroquinolones?

Class C
Avoid use
Increased risk for bone, joint, tendon defects

How do elderly rx to fluoroquinolones?

Tendon rupture is more common

What causes antibacterial drug resistance?

- Overused, overprescribed, improperly taken
- MDR (multiple-drug resistant) AKA superbugs cause superinfections
- Ex: MRSA, S. pneumoniae

Name the parts of a virus:

Capsid
Nucloic acid (DNA or RNA)
Sheath
Rod
Tails

Virus:

- Intracellular, submicroscopic parasites that must infect a living cell to reproduce
- Two types: common & retrovirus

What is the intended response of antiviral therapy?

- shorten duration or intensity of an existing viral disease
- prevent reactivation of a dormant viral infection
- prevents a viral infection from multiplying to point of disease

**must be taken exactly as prescribed**

Do antivirals kill viruses?

No. Virustatic

When do more serious allergic rx to antivirals happen?

With IV admin

How do acyclovir and valacyclovir work?

Slows viral reproduction

Tx: Epstein-Barr, CMV, herpes type 1 & 2, varicella-zoster (chickenpox)

Side effects acyclovir and valacyclovir

Headache
Dizziness
N&V

Adverse effects acyclovir and valacyclovir

DEC kidney function
Kidney dmg
Kidney failure

Before admin acyclovir and valacyclovir:

- Ck if pt is taking anticonvulsants (especially phenytoin)
- Ck IV

After admin acyclovir and valacyclovir:

Infuse over 60 min via IV
Give full glass of water
Push fluids

What do you teach pts about acyclovir and valacyclovir?

INC fluids

How do children rx to acyclovir and valacyclovir?

Oral dosages for children older than 2 are similar to adult dose

How do elderly rx to acyclovir and valacyclovir?

Dizziness, agitation, confusion - side effects
Ck kidney function frequently
No driving or operating machinery until the drug's affects are known

How do amatadine and rimatadine work?

Block the uncoating of the influenza A virus, stopping release of viral particles
into respiratory epithelial cells; prevent infection

Side effects of amatadine and rimatadine:

dizziness
blurred vision
dry mouth
hallucinations
orthostatic hypotension

Adverse effects of amatadine & rimantadine:

(amantadine) – affects CNS; may worsen glaucoma, urinary
retention

Before admin amatadine & rimantadine:

Ck presence of glaucoma, urinary retention, psychiatric problems (esp. depression with
attempted suicide)

Ribavirin does what?

• Suppresses viral action and reproduction
• Used for viral infections that do not respond to other antiviral agents:
– Examples: Hantavirus, hepatitis A and C, respiratory syncytial, West Nile virus

What do you teach pts about amatadine & rimatadine?

– Do not stand or sit up quickly; may rapidly lower blood pressure, causing dizziness and
increased risk for falls
– Hold onto railings when going up or down steps
– Report to prescriber any worsening of depression or thoughts of suicide

How do preggers/breastfeeding rx to amatadine & rimatadine?

Class C
Excreted in breastmilk

How do elderly rx to amatadine & rimatadine?

– Reduce dosage for patients older than 65 years
– Can worsen heart failure and increase edema
– Weigh daily; report gain of >3 pounds in 2 days
– Measure pulse at least once daily; report if irregular or hard to find

Side effects ribavirin:

– Nausea/vomiting, diarrhea, fever, headache, rash, conjunctivitis, muscle pain, fatigue, dizziness, runny nose, injection site pain or irritation

Adverse effects ribavirin:

– Teratogenic
– Prolonged use may impair functioning of liver, kidneys, heart, ears. May lead to some forms of cancer.

Before admin ribavirin:

Check:
– Hearing; cardiac, respiratory, neurologic, kidney, liver functioning
– Blood counts and vital signs

After admin ribavirin:

Check
– Signs of side effects or organ toxicity

What do you teach your pt about ribavirin?

– Take 1 hr before or 2 hr after antacids
– Contact prescriber if symptoms of allergy or other adverse effects develop

How do elderly rx to ribavirin?

– Administer cautiously due to age-related organ changes increasing toxicity risk
– May need lower dosage
– Assess for anemia

How do preggers/breastfeeding rx to ribavirin?

– Category X
– Two forms of contraception

How do oselamivir & zanamivir work?

• Inhibit the enzyme neuraminidase
• Prevent and treat influenza

Side effects of oselamivir & zanamivir

N&V
Diarrhea
Dizziness
Headache

Adverse effects of oselamivir & zanamivir

Rare

What do you teach pts about oselamivir & zanamivir

– Take oseltamivir within 12-48 hr of onset of first symptoms
– Take zanamivir within 12-36 hr of onset of first symptoms
– Discontinue if adverse effect occurs

Retroviruses:

• Always use RNA as its genetic material
• Allow high efficiency of cellular infection
• Human immune deficiency virus (HIV)

HIV & AIDs method of action and distribution:

• HIV attacks the immune system
• Most severe form of immune deficiency disease caused by HIV infection is
acquired immune deficiency syndrome
• Everyone with AIDS has HIV infection
• Not everyone with HIV infection has AIDS
• Opportunistic infections

What are the six classes of antiretroviral drugs?

• Nucleoside analog reverse transcriptase inhibitors (NRTIs)
• Non-nucleoside analog reverse transcriptase inhibitors (NNRTIs)
• Protease inhibitors (PIs)
• Fusion inhibitors
• Entry inhibitors
• Integrase inhibitors

How does antiretroviral tx work? Admin?

• Virustatic
• Given in “cocktails”
– Highly active antiretroviral therapy (HAART)
• Drug resistance common; related to missed drug doses

How do you know if antiretroviral tx is working?

Measured by “viral load” and decreased opportunistic infections

How to NRTIs work?

Inhibit reverse transcriptase and viral DNA synthesis, slowing viral reproduction

Side effects of NRTIs:

nausea, headache, GI upset with fatty or fried foods

Adverse effects of NRTIs:

liver toxicity, peripheral neuropathy with long-term use

What do you teach pts about NRTIs?

– Avoid fatty foods and fried foods
– Loss of sensation increases risk for injury
– Stop abacavir if flu-like symptoms develop

How do children rx to NRTIs?

– All children who are HIV-positive should take
NRTIs as part of HAART
– Dosages for small children usually based on

How do preggers/breastfeeding rx to NRTIs?

– Increased risk for lactic acidosis in pregnancy

How do elderly rx to NRTIs?

– Peripheral neuropathy develops more quickly
– Teach tips to prevent injury

How do NNRTIs work?

• Disrupt HIV reproduction

Side effects of NNRTIs?

rash, nausea/vomiting, headache, abdominal pain, difficulty sleeping, vivid dreams
or nightmares

Adverse effects of NNRTIs?

Anemia
Liver toxicity

What do you teach pts about NNRTIs?

– Notify prescriber of adverse reactions
– Take at least 1 hr before or 2 hr after antacids
– Keep all medical appointments
– St. John’s wort greatly reduces NNRTI effectiveness

How do children rx to NNRTIs?

– All children who are HIV-positive should take NNRTIs
as part of HAART
– Anemia more likely

How do preggers/breasfeeding rx to NNRTIs?

– Etravirine and nevirapine – category B; may be taken
at any stage
– Delavirdine and efavirenz – do NOT take during
pregnancy

How do elderly rx to NNRTIs?

– Drug interactions more likely; report all drugs to prescriber
– Teach how to take pulse and assess for/report irregularities

How do PIs work?

Prevent viral replication and release of viral particles

Side effects of PIs?

headache, diarrhea, depression, difficulty sleeping, abdominal weight gain

Adverse effects of PIs?

– Liver toxicity increased lipid levels
– Uncontrolled bleeding in patients with hemophilia
– Atazanavir and ritonavir can impair electrical conduction
– Darunavir and fosamprenavir contain sulfa

What do you teach your pts about PIs?

– Do not crush or chew capsules
– Check pulse twice daily for a full minute
– Do not take with St. John’s wort

How do children rx to PIs?

– HIV-positive children older than age 6 years take PIs
as part of HAART
– Dosages for older children are nearly the same as for
adults
– Optimal dosages are unknown for infants and children
younger than age 6 years

How do elderly rx to PIs?

– Drug interactions more likely; report all drugs to prescriber
– Teach how to take pulse and assess for/report irregularities

How do fusion inhibitors work?

• Enfuvirtide (Fuzeon)
• Block viral docking protein from fusing with host cell

Side effects of fusion inhibitors:

injection site reaction, constipation, trouble sleeping, depression,
muscle aches

Adverse effects of fusion inhibitors:

peripheral neuropathy, increased respiratory infections (including
pneumonia), liver toxicity

What do you teach pts about fusion inhibitors?

– Storage, handling, and self-injection of drug
– Signs and symptoms of respiratory infection

How do children rx to fusion inhibitors?

– Drug dosages for children 6 years and older based on
weight
– Dosages for children younger than 6 years not established
– Injection site infections occur more often in adolescents

How do preggers/breastfeeding rx to fusion inhibitors?

– Category B
– Begin enfuvirtide therapy in second trimester

How do elderly rx to fusion inhibitors?

– Vision or mobility problems may complicate
self-administration of the drug
– Include family members in teaching self-administration

Entry inhibitors do what?

• Maraviroc (Selzentry)
• Block the CCR5 receptor on CD4+ T-cells

Side effects of entry inhibitors:

muscle aches and pains, cough diarrhea dizziness trouble cough, diarrhea, dizziness, sleeping

Adverse effects of entry inhibitors:

hypotension, liver toxicity

What do you teach pts about entry inhibitors?

– Do not crush or chew capsules
– Practice safety regarding low blood pressure

How do children rx to maraviroc?

Not approved in <16 yo

How do preggers/breastfeeding rx to maraviroc?

– Category B
– Begin maraviroc in second trimester

How do elderly rx to maraviroc?

– Orthostatic hypotension more likely
– No driving or operating machinery until the drug’s effects are known

How do integrase inhibitors work?

• Raltegravir (Isentress)
• Inhibit the enzyme integrase

Side effects integrase inhibitors:

primarily diarrhea

Adverse effects integrase inhibitors:

anemia
hyperglycemia
rhabdomyolysis

What do you teach pts about integrase inhibitors?

– Do not crush or chew tablets; take with food to decrease GI side effects
– Report muscle pain and weakness to prescriber
– Report symptoms of anemia

How do children rx to raltegravir?

– Not approved for use in children younger than 16 years

How do preggers/breastfeeding rx to raltegravir?

Class C

How do elderly rx to raltegravir?

– More likely to take “statin” type of lipid-lowering drugs

Week Three - Lecture (No. 2 - no class last week)

Nursing 308 with Blakely at Capital University

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