1-6 STARRED FLASHCARDS
What is the action of Abx drugs?
Affect target organisms structure, metabolism, or life cycle
What is the goal of Abx medications?
To eliminate the pathogen
What is bactericidal and bacteriostatic?
-cidal: Kill bacteria
-static: Slow growth of bacteria
What may antibiotics be used for?
Prophylactic treatment of people with suppressed or compromised immune systems
Why not just prescribe a really strong Abx?
A. delay effective treatment (YES)
B. Give the bacteria more time to grow (YES)
C. Contribute to the development of drug-resistant bacteria (Yes)
What should the patient know when taking Abx? (12 things)
finish all abx
do not share
keep away from children
educate about decrease of OCP
when to take with food or when to avoid certain ones
teach clients to wear medic-alert bracelets if allergic
Take probiotics (1-2x/day) to counter antibiotic
monitor for hypersensitivity with first dose
know S&S of allergic rxn
MOST abx taken on empty stomach
Assess renal/hepatic function
assess for persistent diarrhea in children
What is the role of the nurse in Penicillin therapy (4)
Assess previous drug runs to penicillin
avoid cephalosporins if pt has severe penicillin allergy (cross sensitivity)
monitor for hyperkalemia and hypernatremia (increases risk in pt with DM or on dialysis)
Monitor cardiac status, including ECG changes
Role of the nurse in cephalosporin therapy?
Assess for presence or Hx of bleeding disorders (ceph reduces prothrombin levels)
Assess renal/hepatic function (esp in elderly)
assess for persistant diarrhea in children
avoid alcohol (some cause disulfiram rxn w/alcohol)
Role of the nurse in tetracycline therapy
Photosensitivity may result
do not take with milk products, iron supplements, magnesium containing laxatives, or antacids
watch for supra infection such as pseudomembranous colitis
Role of the nurse in Macrolide therapy?
Watch liver with EES erythromycin estolate
multiple drug-drug interactions occur with macrolides (CYP)
monitor - exacerbates heart disease
cause a metallic taste in mouth
Aminoglycosides are
More toxic than most abx
have potential to cause serious ADEs (ototoxicity, nephrotoxicity, neuromuscular blockage)
last names dont work with this family and macrolides
Ototoxicity is worse if given with?
Lasic
Nephrotoxicity is worse If given with
Zovirax
Neuromuscular blockage includes
Respiratory paralysis
Fluoroquinolones are decreased how much and with what
decreased 90% if taken with multivitamins or minerals such as calcium, magnesium, iron, or zinc ions
Decreased 50% is taken with tetracyclines
Important things with fluoroquinolone
IV = PO and therefore easy transition to home
NO teenager/athletes: Tendon rupture
Can Cause C diff
QT prolongation/arrhythmias (IRR vs RRR)
Role of the nurse in fluoroquinolone therapy?
Norfloxacin may cause photophobia
teach that drug may affect tendons, esp in children
monitor for dysrhythmias
crosses into breast milk
Sulfonamides
Widespread use has lead to increases resistance and decreases usage/Rx
used in combo to trat UTIs
anti-inflammatory properties of sulfonamide component can help with RA and ulcerative colitis
teratogenic
do not take breast feeding/pregnant
caution rxn to sulfonamide abx could mean allergy to other sulfonamide medications
allergy to these meds may cause sensitivity to abx - caution with first dose
What is the role of the nurse in sulfonamide therapy
assess for anemia/other hematological disorders
assess renal function (may increase risk for crystalluria)
alterante form of BC
Vancomycin MOA
Bactericidal, inhibits cell wall synthesis
Vancomycin primary use
reserved for severe or resistant gram positive infection, effective for MRSA infections, used to treat C diff
Vancomycin ADEs
ototoxicity
nephrotoxicity
red man syndrome
confusion/hallucinations
anaphylaxis
What is acquired resistance
as abx are used, they destroy sensitive bacteria
What bacteria stays following acquired resistance
only insensitive mutated bacteria remain
1. free from competition from sensitive bacteria (mutated thrives
2. pt now develops infection that is resistant to drug
3. resistant bacteria can be transmitted to others
ARO’s
Carbapenem resistant enterobacteriaceae
extended spectrum B lactamase
MRSA
VRE
VRSA
what will MRSA not respond to
fluoroquinolone, macrolides, ahminoglycosides or tetracyclines
What is multi drug resistant
when an organism is resistant to more than one drug
what do abx not treat
viral infections
What is a superinfection
host flora killed by abx, MO’s multiply
S&S of superinfections
Diarrhea
bladder pain and painful urination
abnormal vaginal discharge
red rash with satellite lesions
What are some considerations for patients taking abx
inform as to SE (skin teeth tendons ears kidneys)
assess renal/hepatic function
assess for persistent diarrhea in children
take probiotics to counter
wear medic alert bracelets if allergic
know S&S of allergic rxn
Fungal infections characteristics
Not easily transmitted through casual contact
Love dark, moist environments + lots of sugar
serious fungal infection uncommon in healthy individuals
treatment may require weeks to months of therapy due to resistance
Fungal infections in immunocompromised pts
systemic fungal infections may be rapidly fatal
may experience frequent fungal infections and require aggressive pharmacotherapy
Nystatin drug interactions/treatment of OD
Drug interactions unknown
Treatment of OD: symptomatic
Nystatin considerations
Hx and assessment (observe for improvement and report of persistent infections)
Avoid occlusive dressings or ointment on moist dark areas of body
teach pt to avoid sharing shoes, towels, or personal objects
What drugs are similar to nystatin
Griseofulvin
What is griseofulvin used for
skin infections like lock itch, athletes foot, ringworm, and fungal infections of scalp, fingernails and toenails
Griseofulvin SE
phototoxicity
SJS
urticaria
dizziness
decreased OCP
alcohol=disulfiram like rxn
When in doubt
check BG (not feeling well, back from exam and didnt eat, sweating or confused)
What to watch for with beta blockers?
Hypoglycemia, beta blockers mask the S&S of hypoglycemia
What are the rapid insulin therapies
- Insulin aspart
more rapid onset of action and shorter duration of action than regular insulin - Insulin glulisine
rapid onset and short duration (3 to 5 hrs)
given by SC injection only - Insulin Lispro
rapid acting analog of regular insulin
helps control the rise in BG brought on by a meal
not given IV; often used with infusion pumps
Rapid acting onset, peak duration
Onset: <15 min
Peak: 0.5 to 1 hr
Duration: 3-4hrs
BEST TO BE EATING
Humulin Regular insulin ADEs/Serious ADEs
ADEs:
irritation at site
lipodystrophy
weight gain
serious ADEs:
hypoglycemia
rebound hyperglycemia
hypokalemia
Insulin therapy considerations
Medicine Hx (herbs and dietary supplements)
alcohol intake and BG
consumed or capable of consuming food before administration
only regular insulin intravenously
assess pts knowledge + educate
do not administer when BG less than 4 mmol
rotate injection sites
check periodic hemoglobin A1C levels
assess for DM complications (eyes heart kidneys feet)
Role of the nurse in insulin therapy
be familiar with onset, peak and duration of action of prescribed insulin
be aware of important aspects of each specific insulin
not all types of insulin are compatible (clear before cloudy)
know S&S of hypoglycemia and hyperglycemia
Considerations for all Oral Diabetic Agents
Monitor BG
Check for S&S of illness or infection
watch liver function
assess for adherence tp therapy, and the ability for self care
sulfonylureas contraindicated in women who are pregnant or breast-feeding, or persons with renal or liver disease
second generation sulfonylureas have fewer drug-drug interactions
Sulfonylureas
increase stimulates insulin release from pancrease
increase sensitivity to insulin receptors
decreased chance of prolonged hypoglycemia
10% experience decreased effectiveness after prolonged use
most SE are minor an GI related
Sulfonylureas contraindications/precautions
sensitivity to self drugs to thiazide diuretics
renal or hepatic disease
if used during pregnancy, discontinue at least 1 month before delivery
Sulfonylureas drug interactions
alcohol
oral anticoagulants, MAOIs, probenecid, sulfonamides
chloramphenicol, salicylates, clofibrate
rifampin
thiazides, sulfonamide based drugs
ginseng, garlic, black cohosh, juniper berries, fenugreek, coriander, dandelion root
Biguanides
decreased glucose production by liver
increase insulin sensitivity at tissues
improve glucose transport into cells
do not promote weight gain
usually first line of treatment
6-12 weeks to reach therapeutic effect
need to be held 48 hrs prior and 48 hrs after a pt needs contrast dye to prevent lactic acid build up
Biguanades contraindications/precautions
impaired renal function
HF, liver failure, Hx of lactic acidosis
concurrent serious infection
any condition that predisposes pt to hypocemia
anemia, D/V, dehydration, fever, gastroparesis, GI obstruction
hyperthyroidism, pituitary insufficiency, trauma
pregnancy/lactation
Cholinergic Medications medicinal uses
Neurogenic bladder
urinary retention
BPH
Glaucoma
Myasthenia Gravis
Alzheimers
Cholinergic medications S&S of toxicity
SLUDGE
Salivation
Lacrimation
Urinary incontinence
Diarrhea
Gastrointestinal cramps
Emesis
What is physostigmine used for
an antidote for anticholinergic poisoning and common pesticide poisoning
Anticholinergic medications
can be natural like scopolamine and atropine or synthetic like benztropine, dicyclomine, oxybutynin, toleradine, glycopyrrolate
To be used cautiously in the geriatric population (esp in males with BPH and urinary retention)
Anticholinergic medications considerations
Watch for contraindication in long term usage
sensitivity to light
dry mouth
agitation
blurred vision
high risk of heat stroke in geriatric patients
stress fluids and a high fibre diet
teach pt when to call HCP
Adrenergic medications medicinal use
Dobutamine (agonist) increase contractility and elevate BP
phenylephrine (agonist) causes vascular constriction in nasal arteries, dries up nasal drip and mucous
Atenolol (antagonist) slows HT and drops BP (not as cardio selective as metoprolol so watch with asthmatics)
Emergency drugs
dopamine - dose dependent
dobutmaine
norepinephrine
epinephrine - protect from light
Adrenergic considerations
major SE of B agonists is cardiac arrhythmia
these drugs increase myocardial O2 demand and can precipitate engine - avoid in CAD - do not give with MI
avoid caffeine
headache and tremor also common but call HCP is nervousness/jitters or palpitations
alpha 1 adrenergic antagonists are used for BPH (relaxes smooth muscle and urinary retention
assess vital signs prior to administration - previous 12 lead ECG, HR, Heart Hx heart sounds, RR, O2 sat, need for O2, breath sounds, resp effort, skin colour
Cholinergic agonists when not to use
GI/GU obstruction
bradycardia
epilepsy
hypotension
COPD
parkinsons disease
Adrenergic agonists when not to use
Narrow angle glaucoma
tachycardia, arythmies or HTN
liver disease
enlarged heart
disorders of arteries and veins
disorders affecting the blood supply to the brain
Catecholamines
Short duration of action
destroyed rapidly by MAO and COMT
no PO - parenteral or inhalation d/t COMT in the intestinal tract
do not cross BBB
Noncatecholamines
May be taken PO
not destroyed as rapidly
better able to enter brain and affect CNS
Epinephrine considerations
assess for underlying problem/pre existing conditions
Hx/Px (VS)
closely monitor resp status
use cardiac monitor/resuscitation equipment
monitor BP closely
inform prescriber of changes in I&O
monitor for hyperglycemia - insulin gtt
examine ocular and nasal mucosa
protect from light (store rip in dark place, brown bag/IV)
Phenylephrine contraindications/precautions
severe HTN
pre existing bradycardia
advanced CAD
nitroglycerin
narrow angle glaucoma
hyperthyroidism
diabetes
Phenylephrine treatment of OD
Phentolamine
anti-dysrhythmic drugs
Phenylephrine Considerations
examine IV sites frequently
advise pt to remove contact lenses
dark eye protection after ophthalmic administration
avoid caffeine (with all adrenergic agonists)
contact HCP is palpitation or jittery/nervousness
Muscarinic antagonists uses
GI disorders such as IBS
ophthalamic procedures
cardiac rhythm disorders
chemotherapy induced diarrhea
adjuncts to anesthesia
asthma and COPD
antidotes for poisoning or OD
Urge incontinence (overactive bladder)
Parkinsons disease
Muscarinic antagonists ADEs
Urinary retention
xerostomia
tachycardia
CNS stimulation
Dry eyes
photophobia
urinary retention in BPH
Anticholinergic syndrome
dry mouth
difficulty swallowing
visual changes
blurred ision
photophobia
agitation and hallucinations
Nicotinic Antagonists
Motor end plate of muscle causes release of Ach to travel to receptors on skeletal muscle = muscle contraction
continous depolarized state in which calcium does not return to its storage depots
Succinylcholine uses
surgical anesthesia
pseusocholinesterase
relaxes abdominal muscle, or for relaxation prior to intubation
induces relaxation in less than 1 minute
muscle strength returns quickly after discontinuation of the drug
patients can still feel pain and is aware of surroundings - benzos and opioids
Succinylcholine ADEs
complete paralysis of diaphragm/intercostalk muscle
tachycardia
hypotension
urinary retention
Succinylcholine serious ADEs
malignant hyperthermia - muscles rigid, skin hot
resp depression
apnea
dysrhythmias
Tubocurarine
nondepolarizing neuromuscular blockers
used to relax skeletal muscles during surgical procedures
do not cause sedation, analgesia, or LOC - must use Enzo’s, propofol, and opioids
First dose phenomenon
When the SNS is blocked, the parasympathetic predominates resulting in hypotension or orthostatic hypotension (decreased blood flow to brain = syncope)
prevention by initial therapy begun with low doses and usually given at bedtime
reflex tachycardia and nasal congestion also occur
Selective alpa 1 blockers
block peripheral catecholamines
relax smooth muscle of bladder and prostate
increases urine flow
alpha 1 blockers action on arterioles
block vasconstriction on vascular smooth muscle (afterload) which decreases BP directly
Alpha 1 blockers action on veins
Block vasoconstriction which decreases venous return (preload) to heart and lowers BP indirectly
What can alpha blockers be used with
diuretics
selective alpha 1 blockers uses
benign prostatic hyperplasia
phenochtomocytoma
HTN
Benign prostatic hyperplasia
two selective agents used
1. Alfuzosin
2. Tamsulosin
Pheochromocytoma
Small tumour of adrenal medulla causing irregular secretion of Epi and NE
- excessive secretion of catecholamine in this condition causes severe HTN
Selective Beta-Adrenergic Antagonists
Block only beta 1 receptors
cardioselective
fewer non cardiac SE
little effect on bronchial smooth muscle
can be safely given to clients with asthma and COPS
Nonselective beta-ldreergic antagonists
block beta 1 and beta 2 receptors
produce more SE than selective beta 1 antagonists
serious SE is bronchoconstriction - caution in pts with COPD or asthma
Beta adrenergic antagonists uses
most actions relate to CV system
- slow conduction velocity through AV node
- decrease HR (chronotropic)
- decrease force of contractions (inotropic)
during stress/exercise - prevents normal sympathetic stimulation o heart
cautions when administering CCBs concurrently as may potentiate HF
ADE’s of beta blockers?
prevent hyperglycemic effect of catecholamine
pts with DM can cause hypoglycemia and mask the signs
decreased amount of free fatty acids available during metabolic stress
bronchoconstriction (No pts COPD or asthma)
rebound cardiac excitation if BBs withdrawn abruptly
educate patient to never stop without talking to HCP first
Propranolol considerations
monitor VS Q15 min - q1hr
Hx &Px - assess for asthma and COPD
review lab tests for kidney, liver, hematologic, and cardiac functions
watch for ADRs in older adults and in pts with impaired renal function
monitor I&O and take daily weights (esp in HF)
educate regarding decreasing salt intake
examine for impaired circulation (SOB, edema etc)
watch for widening QRS - immediate attention
Types of nonselective beta blockers
Carbedilol - black sheep last name
Labetalol
nadolol
penbutolol
sotalol
timolol
metoprolol considerations
monitor BP and HR frequently during IV administration
have baseline ECG and repeat if telemetry changes or CP
monitor for symptoms of impending HF
record I&O, weight, bilateral breath sounds
take radial pulse - do not administer if HR <60bpm or is SBP <100 (watch for hypotension symptoms)
do not omit, increase or decrease dose
avoid late evening dose
symptoms of depression
masked hyperthyroidism
report visual problems or cold painful feet/hands
caution in DM pts
discontinue drug slowly due to potential rebound effects
do not breast-feed without consulting provider
CCBs myocardial effects
reduces force of myocardial contraction (negative inotropic effect)
- reduces inward movement of calcium during plateau phase of action potential
CCBs cardiac conduction effects
negative chronotropic effect
SA node generates fewer action potential
slows automaticity
decreases HR
Nifedipine Drug Interactions
With drugs that induce or inhibit CYP3A4
additive effects with other antihypertensives
increased risk of CHF with BB
increased serum levels of digoxin - bradycardia
syncope/drop in BP with alcohol
Nifedipine Treatment of OD
Rapid-acting vasopressors such as dopamine or dobutamine
calcium infusions
Verapamil drug interactions
increased digoxin levels = increased bradycardia risk
additive hypotension or bradycardia with other antihypertensive drugs
3x plasma concentration of buspirone
risk of myopathy increased significantly with statins
increases carbamazepine levels = neurotoxicity
grapefruit juice may increase levels
Verapamil considerations
monitor BP before admin and 30 min to 1 hr after and just prior to next dose
withhold is systolic BP <90 or symptomatic
monitor for edna
keep patient recumbent for at least 1 hr after administration
monitor for heart block or bradycardia with digoxin use
monitor I&O
monitor on telemetry continuously if parenteral
Drugs similar to verapamil
Diltiazem
treatment of atrial dysrhythmias and HTN, stable and vasospastic angina
same profile as verapamil
migraine prophylaxis off-label
The stomach
secretes acid, enzymes and hormones that are essential to digestive physiology
Natural defenses of the stomach
Somatostatin
bicarbonate ion
mucus
prostaglandin E2
Prostaglandin antagonists include
NSAIDs/ASA (damages GI mucosa directly)
corticosteroids
Peptic ulcer risk factors
infection with helicobacter pylori
close fam Hx of PUD
drugs (glucocorticosteroids, NSAIDs, platelet inhibitors
Blood group O
smoking
excessive caffeine
psychological stress (thought to be primary cause for many decades)
NSAID induced PUD risk factors
long term use
advanced age
Hx of ulcers
corticosteroids
anticoagulants
alcohol and smoking
H2 receptor antagonists
ranitidine
cimetidine
famotidine
nizatidine
H2 receptor antagonists pharmacokinetic properties
rapid absorption from small intestine
30 min onset of action
half life from 1-4 hours
no known effects on the fetus
excreted primarily from the kidneys
ADEs of antacids
constipation
at high doses aluminum products bind with phosphate in GI tract = long term use can result in phosphate depletion
High risk:
-malnourished
-alcoholics
-renal disease
Contraindications with Antacids
prolonged use with low serum phosphate
avoid with suspected bowel obstruction
Drug interaction with Antacids
dont take with other meds - interfere with absorption
DECREASE
cimetidine, fluoroquinolone, digoxin, isoniazid, cholorowuine, NSAIDS, iron salts, phenytoin, tetracycline, thyroxine
anticholinergic increase effects
aluminum and calcium antacids may inhibit iron absorption
Antacids considerations
PMH
watch kidney lab values
monitor for bowel changes and worsening symptoms
hold drug and notify prescriber if pt symptoms of appendicitis, undiagnosed GI bleeding, or suspected obstruction
Anticholinergic agents and antihistamines N/V
Simple nausea like nausea due to motion sickness
Serotonin receptor antagonists N/V
chemotherapy induced N/V (primary indication for the use of antiemetic medication)
Phenothiazine or hydroxyzine N/V
antineoplastic therapy
Ondansetron therapeutic/pharmacologic
There: Antiemetic
Pharm: serotonin (5-HT3) receptor antagonist
Ondansetron uses
treatment of serious N/V
used at least 30 min prior to chemotherapy and continued for several days after
off-label for cholestatic or opioid-induced pruritic
Ondansetron MOA
Blocks serotonin receptors in teh chemoreceptor trigger zone
Laxative (bulk forming)
promotes defecation
prevents and treats constipation
Saline Cathartic
pulls water into stool
implies accelerated, stronger, and more complete bowel emptying through osmosis
Laxatives treatment
simple chronic constipation
accelerate removal of ingested toxic substances
accelerate removal of dead parasites
cleanse the bowel prior to diagnostic or surgical procedures
Avoid increased colon pressure
possible bowel perforation
monitor for retrosternal pain
Metamucil considerations
know PMHx
assess bowel movement and GI functioning
mix powder and granules with at least 8 ounces of a pleasant tasing liquid immediately before use and drink lots of water
immediately report complaints of retrosternal pain after taking the drug
smaller, more frequent doses spaced throughout the day may be indicated to relieve discomfort
monitor warfarin and digoxin levels closely
ADEs of diphenoxylate with atropine
Dizziness
lethargy/drowsiness
anticholinergic effects of atropine
Considerations of diphenoxylate with atropine
Know PMHx/Sx
perform complete assessment of bowel movements and GI functioning
report abdominal distention and signs of decreased peristalsis to provider
monitor for S&S of dehydration esp with young children
maintain a safe environment because diphenoxylate with atropine may cause drowsiness or dizziness
IBD treatment
5-ASA agents, immunosuppressants, biologic therapies and anti-inflammatory drugs
Goals of IBD drugs
reduce symptoms
keep is remission (immunosuppressive agents)
alyer progression of the disease
