Pharm 103 Test 2 Flashcards
Initial 4 drug combo for TB
Reduces MDRTB: isoniazid rifampin pyrazinamide ethambutal not as common-streptomycin
prophylaxis drugs for TB for ppd + HCWs
isoniazid or rifampin
INH action
inhibit cell wall synthesis
some lack liver enzyme to metabolize
isoniazid
AEs of isoniazid
hepatotoxicity (monitor liver function) peripheral neuritis B6 deficiency (take supplement)
rifampin action
inhibit protein synthesis
causes orange/brown discoloration of body fluids
rifampin
General TB med AEs
Hepatotoxicity (INH, PZA, rifampin)
Kidney issues (INH, Rif, esp streptomycin)
GI upset (take with snack)
eye problems (ethambutol especially: optic neuritis and decreased visual acuity, red-green color
INH)
non-opioid antitussive
dextromethorphan
potential for abuse
antitussive action
suppress cough reflex in medulla to reduce annoying, nonproductive cough
AE of high dose of dextromethorphan
dizziness and sedation
opioid antitussive
codeine
very effective but can be habit forming
AEs of codiene
constipation, sedation, hypotension
antihistamine and antitussive
diphenhydramine
AEs of diphenhydramine
drowsiness, dry mouth, anorexia
alpha 1 adrenergic receptors-location and function
mostly in peripheral arteries and veins; cause vasoconstriction when stimulated
alpha 2 adrenergic receptors-location and function
located on nerve membranes; modulate NE release to prevent overstimulation
beta 1 adrenergic receptors-location and function
mostly heart,some kidney; increase HR, contractility, automaticity, AV conduction and renin release from kidneys
beta 2 adrenergic receptors-location and function
lungs; cause bronchiole smooth muscle relaxation, resulting in bronchodilation
Decongestants-Action
sympathomimetic; shrink engorged nasal mucosa by stimulating alpha receptors of bvs in nasal mucosa causing vasoconstriction, reducing swelling and secretions
systemic effects of decongestants
especially in fragile pts.
cardiac stimulation-irregular rhythm, increased HR
CNS stimulation-DZNS, HA, irritable
Increase BS in DM
decreased sphincter contraction, decreased voiding
Avoid decongestant use in these pts
heart disease, HTN
Hyperthyroid
DM
to avoid systemic effects of decongestants, use
topical nasal spray to avoid cardiac stimulation; steroid nasal spray or mast cell stabilizers to avoid all
nonselective adrenergic agonist
epinephrine
very effective bronchodilator but multiple AEs since stimulates alpha, B1 and B2: jittery, increased HR, increased BP, HA, HTN
only used in acutely ill pt-anaphylaxis
B2 adrenergic agonists-action
mostly stimulate B2 receptors in lungs causing bronchodilation by increasing cAMP; in lg frequent dose can stimulate B1 (increase HR)
AE of B2 agonists
tremors, anxiety, minimal tachycardia and increased bp, arrhythmia in some pts.
fast acting B2 agonists–rescue meds in MDI or neb
albuterol (duration 3-4h) and levalbuterol (longer duration-8h)
long-acting B2 agonists (bid)
Brovana (neb)
salmeterol (Serevent)
formoterol (Foradil)
B2 agonist that can be used to stop preterm labor
terbutaline (Brethine)
Advair diskus
Dry powder inhaler-B2 agonist and steroid
salmeterol (Serevent) and fluticasone
daily use-bid
Combivent inhaler
ipratropium (Atrovent) and albuterol
used in COPD
DuoNeb in nebulizer
Symbicort
budesonide and formaterol
similar to Advair- steroid and long acting B2 agonist
two MDIs that combine a steroid and a long-acting B2 agonist
Advair diskus and Symbicort
PSNS stimulation in lungs causes
bronchoconstriction–need anticholinergic med
anticholinergic bronchodilators
ipratropium (Atrovent)–short acting and duration
tiotropium (Spiriva)–longer acting (qid)
Leukotriene receptor antagonists-action and examples
leukotrienes cause bronchoconstriction–these meds stop that part of the inflammatory process
Long term preventative of acute asthma problems
montelukast (Singular)
many interactions, not 1st choice
Xanthine bronchodilators-action and examples
stop cAMP from breaking down, promoting bronchodilation
oral theophylline/aminophylline
related to caffeine, AEs: tachycardia, nervousness
monitor blood levels, can become toxic
Inhaled Corticosteroids used for long term prevention in asthma and COPD (not rescue)
fluticasone (Flo-vent)
budesonide (Pulmicort)
triamcinolone (Asmacort)
beclomethasone (Beclonase)
inhaled steroids used for asthma instead of oral/IV because
less systemic AE
may use oral or IV in acute situation
Mast cell stabilizers-action and examples
prevent mast cells from releasing inflammatory mediators
cromolyn (Intal)
nedocromil (Tilade)
three functions of respiratory aerosols
Decongest, liquify secretions
Bronchodilate, topical med admin
moisten, heat or cool resp mucosa
DPIs
dry powder inhalers
Advair and Spiriva
Effects of histamine release in inflammation
dilates and increases permeability of nasal capillaries causing edema
constricts smooth muscle in lungs
increases GI secretions
anti histamines action
block histamine receptors so histamine can’t bind-don’t effect already bound histamine
1st vs 2nd generation antihistamines
1st gen-Benadryl AEs:drowsiness, decreased coordination, allergic rxns, n/v
2nd gen-nonsedating antihistamines
Secondary uses for diphenhydramine
n/v, vertigo, sleep aid
muco-kinetic vs. muco-lytic
muco-kinetic: thins mucus for better ciliary action (ex. aerosolized saline, water)
muco-lytic: chemically breaks down mucus
guanifenesin, Mucomyst
3 uses for acetylcysteine (Mucomyst)
- To reduce tenacity and viscosity of thick secretions, esp. in CF
- Antidote for tylenol OD-blocks livery toxicity from tylenol
- Protects kidneys from damage when IV contrast is used in pt with renal dysfunction
Quick relief agent bronchodilators
albuterol MDI/neb
ipratropium (Atrovent) MDI
oral prednisone (not as much)
anticholinergic bronchodilators (2)
ipratropium (Atrovent)
tiotropium (Spiriva)
alpha adrenergic blockers-action
HTN med; block alpha 1 receptors in peripheral arteries and veins that cause vasoconstriction; preventing stimulation dilates arteries and veins, decreasing arterial pressure and venous return to the heart, decreasing CO and bp
there are selective and nonselective
selective alpha adrenergic blockers
HTN med; block only alpha 1 receptors -sin prazosin (Minipress) terazosin (Hytrin) doxazosin (Cardura)
alpha adrenergic blocker that can be used in treatment of BPH
terazosin (Hytrin)
nonselective alpha adrenergic blockers
block E and NE, alpha 1 and alpha 2 used to treat HTN d/t pheochromocytoma tumor of adrenal medulla in which too much E and NE are released phenoxybenzamine (Dibenzyline) phentolomine (Regitine) used in treat
nonselective alpha blocker used to treat increased alpha activity disorders (Raynauds, frostbite) where there is too much vasoconstriction
phenoxybenzamine (Dibenzyline)
nonselective alpha blocker used to reverse tissue necrosis when drugs extravasate
phentolomine (Regitine)
AEs of alpha blockade
most important: orthostatic HoTN
can go away eventually, get OOB slowly
S=syncope and dizziness (OHoTN), sexual dysfunction
I=Increased HR, weakness,
N=nasal congestion
Centrally-acting alpha 2 stimulators-action and examples
suppress SNS outflow in brainstem to heart and bvs and decrease renin from kidneys (alpha 2 receptors modulate NE release to prevent overstimulation)
clonidine (Catapres)
methyldopa (Aldomet)
centrally-acting alpha 2 stimulators and direct-acting vasodilators are usually given with a diuretic because they can cause
Na and water retention
centrally-acting alpha 2 stimulator AEs
drowsiness, sedation
decreased concentration depression
dry mouth
This centrally-acting alpha 2 stimulator can cause severe rebound HTN if stopped abruptly
clonidine (Catapres)
This centrally-acting alpha 2 stimulator can cause hemolytic anemia, liver toxicity, and dark urine
methyldopa (Aldomet)
Direct-acting Vasodilators-action and examples
decrease bp by dilating arterioles (not veins)
hydralazine (Apresoline)
minoxidil (Loniten)
often given with diuretics, can cause Na and fluid retention
Beta Blockers-action
nonselective and cardioselective
decrease O2 demand of heart by blocking SNS response
decrease HR (increases filling time of ca’s)
and contractility, resulting in decreased CO and myocardial O2 demand
decreased AV conduction
prevent renin release from kidneys
decrease PVR long term
-olols
mostly widely used drug for HTN
Beta Blockers
two types of Beta Blockers
nonselective (block B1 and B2)
cardioselective (block B1 only)
cardioselective don’t cause bronchospasm like nonselective can
nonselective Beta Blockers
propanolol (Inderol)
nadolol (Corgard)
Timolol (Blocadren)
cardioselective Beta Blockers
atenolol (Tenormin)
metoprolol (Lopressor)
danger in cardioselective Beta Blockers for DM pts
may mask “jitters” and effects of hypoglycemia
don’t use nonselective Beta Blocker in asthma pt because
may cause bronchospasm
Newest Beta Blocker, blocks B1 and vasodilates with endothelium derived NO
nebivolol (Bystolic)
Beta Blockers can treat tachyarrythmias because they
decrease rate of AV conduction
Beta Blockers are less effective in
blacks
B1 adrenergic receptor stimulation increases (5)
HR contractility automaticity AV conduction Renin from kidneys (activation of RAAS)
B2 adrenergic receptor stimulation causes (2)
Bronchodilation
Increased breakdown of glycogen into glucose
do not stop Beta Blocker use abruptly because
sudden withdrawal can exacerbate angina by rebound vasoconstriction
Combined alpha and beta blocker-action and examples
Block A1: promote vasodilation
Bock B1: decrease HR and contractility, decrease renin release in kidney
labetalol (Normodyne)
carvedilol (Coreg)
Major AE of combined alpha and beta blocker
Orthostatic Hypotension and Bradycardia
AEs of Beta Blockers
Bradycardia, worsening HF
weakness, lethargy
sexual dysfunction
depression, insomnia, bizarre dreams
may delay recovery from hypoglycemia in Type 1 DM
nonselective only: may promote bronchospasm and bronchoconstriction
Calcium channel blockers-action and types
prevent Ca from entering myocardial cells, decreasing force of myocardial contraction
results in: coronary artery dilation and peripheral artery dilation; some decrease conduction
Anti-HTN: nifedipine (Procardia) and amlodipine (Norvasc)
Antianginals and antiarrythmics (cardiosuppresive): verapamil (Calan)
Intermediate acting: diltiazem (Cardizem)
anti-HTN CCBs
nifedipine (Procardia)
amlodipine (Norvasc)
antianginal and antiarrythmic (cardiosuppressive) CCBs
verapamil (Calan): most conduction reducing b/t SA and AV; some vasodilation
diltiazem (Cardizem): intermediate acting bt conduction reducing and vasodilation, reducing HTN
Use diltiazem or verapamil cautiously with
bradycardia, HF, AV block
bc both decrease donduction
AEs of CCBs
constipation HoTN dizziness, HA skin flushing edema
ACE inhibitors-action and examples
blocks conversion of Ag I to Ag II, a potent vasoconstrictor. Promotes relaxation of arteries and excretion of Na and H20. Drug of choice for HTN and CHF.
captopril (Capoten)
enalapril (Vasotec)
lisinopril (Zestril)
AEs of ACE inhibitors
first dose HoTN
persistent dry cough
hyperkalemia (watch for gradual increase)
Danger of angioedema
angioedema-definition and what drugs can cause it
ACE inhibitors
histamine response causing edema of mucus membranes of lips, tongue, and glottis.
Stop drug immediately and give epinephrine
Angiotensin II Antagonists (Angiotensin Receptor Blockers)-action and examples
newer, similar to ACE I but don’t cause cough
Block AG II from binding to receptors on bvs and kidneys, promoting vasodilation and reduced bp, promoting excretion of Na and H20
losartan (Cozaar)
irbesartan (Avapro)
AE of ARB’s
URI and HA
ARBs can help HF because
decreased bp makes it easier for the heart to pump
3 meds used to treat angina
CCBs
BBs
nitrates
no grapefruit juice with
CCBs
If there are no written parameters, hold a BB for
SBP < 120
HR < 60
closely watch BS in DM pts on
Beta Blockers
oral diabetic meds and insulin can delay effects also
first choice in acute angina attack
nitroglycerine
rapid and long term treatment of angina; treats HF also
nitroglycerin-action
relax smooth muscle cells around arteries and veins to dilate them; this decreases BP and cardiac workload
dilate ca’s -decrease angina
dilate peripheral a’s - decrease afterload
dilate veins-decrease venous return and preload
Hypertensive crisis can result if using erectile dysfunction med with
nitroglycerin
when giving SL nitro, assess BP and HR when
before giving and 5 minutes after
AEs of nitroglycerin
orthostatic HoTN
flushing
dzns, weakness
HA-expected, give tylenol
Inotropes alter
force of heart contraction
chonotropes alter
rate of heart contraction
dromotropes alter
rate of conduction SA to AV
Digoxin (Lanoxin) action
alters ion movement across myocardial PM
positive inotropic (increase strength of contraction) which increases emptying
negative chono and dromotropic (decreased rate of contraction and conduction) which increases filling
Overall: increased CO, perfusion, blood to kidneys and excretion
decreased pulmonary and systemic congestion
Digitalization
pt given loading dose of dig to saturate body tissues with med and get high blood levels. Followed by maintenence dose until pt is at therapeutic level.
Digoxin given to treat
Afib, Aflutter, CHF (4th line tx, used to be 1st)
Therapeutic level for Digoxin
0.8-2.0 ng/mL (less in renal pts)
small therapeutic index, and some pts can be toxic at therapeutic level
most common cause of dig toxicity
hypokalemia
s/s digoxin toxicity
fatigue
blurred vision
disturbed color vision (yellow/green halos around objects)
GI disturbance-n/v, anorexia, abd pain diarrhea
CNS-DZNS, confusion, delerium, depression
change in HR, arrythmias
Hyperkalemia
Times to measure dig level
digitization post op renal failure pt showing s/s toxicity intervals in treatment
pt teaching about dig
always take apical HR before taking med
inform MD of GI or visual complaints
eat food high in K
Dig antidote
Digibind–antibody that binds digoxin and inactivates it
drugs that increase risk of digoxin toxicity
antacids, calcium preps
K wasting diuretics, steroids, some abx–all these 3 can cause hypokalemia
AEs of digoxin are related to
dose; continnum of s/s toxicity
fatal arrythmias
bradycardia
GI, CNS (can go to seizures and hallucinations)
conditions that may predispose to digoxin toxicity
hepatic/renal impairment
MI/heart disease
electrolyte imbalances (low K)
hypothyroid (decreased metabolism)
Don’t give Digoxin with
antacids, high fiber, or food (one hour before or two hours after meals)
Assess before giving digoxin
electrolytes, renal function
apical and radial HR and rhythm for 1 minute
Short term tx for CHF pt unresponsive to dig
Phosphodiesterase inhibitors (PDI) Inamrinone (Inocor) milrinone (Primacor)
Direct renin inhibitors
block activity of renin enzyme converting Ag I to Ag II
aliskiren
pt teaching about vasodilators includes avoiding (3)
exercise for 3 hours after taking
hot tubs
alcohol
pt teaching about HTN meds includes (4)
low Na diet
OOB slowly
don’t d/c abruptly
contact MD for sexual dysfunction
when giving a HTN med, assess BP
prior to dose (w/in 30 min)
recheck at peak effect time
nifedipine, amlodipine
Procardia, Norvasc
CCBs with no antiarrythmic action, only vasodilation
diltiazem, verapamil
Cardizem and Calan
CCBs with antiarrythmic effects
block Ca channels in heart to decrease conduction
CCBs that treat angina
diltiazem, verapamil, and nifedipine
block Ca channels in bvs, causing coronary artery and peripheral artery dilation
advantage of ARBs over ACE inhibitors
no dry cough, less risk of hyperkalemia
BBs used for angina
atenolol, metoprolol
decrease myocardial O2 demand and workload
decreased HR increases diastole, increases filling time of coronary arteries.s
NO sudden withdrawal from BBs or CCBs because
could cause rebound HTN
oral antidiabetic agents and insulin can delay effects of
BBs and CCBs
used for rapid and long term treatment of angina; vasodilate arteries and veins by relaxing smooth muscle
nitrates
chemical tourniquet
nitrates
organic nitrates, similar to nitroglycerin
isosorbide dinitrate-acute and exertional relief
isosorbide mononitrate-stable angina
Direct Acting vasodilator that can cause lupus-like syndrome (butterfly rash, sore throat, fever, joint pain
hydralazine (Apresoline)
Direct acting vasodilator that can cause pericardial effusion
minoxidil (Loniten)
These meds can increase BS in DM pts
Decongestants
Digoxin is used to treaty
A fib, Aflutter, CHF
Monitor glucose level closely for a DM pt on these meds
BB
Danger of sympathomimetic decongestants in fragile pts
Epinephrine-like effects
Increased HR, irregular rhythm, anxiety, HA, increased BS
Avoid decongestants in pt with
Arrhythmia, HTN, hyperthyroid, DM
Orthostatic HoTN is considered significant if (3)
bp decreases by 20 mm Hg OR
pulse increases by 20 OR
pt c/o dizziness
