Exam 1 Flashcards
(342 cards)
1
Q
enteral
A
absorbed through the GI tract
2
Q
parenteral
A
given outside of the GI tract
3
Q
PO
A
oral
4
Q
PR
A
rectal
5
Q
SL
A
sublingual
6
Q
IV
A
intravascular or intravenous
7
Q
IM
A
intramuscular
8
Q
SC or SQ
A
subcutaneous
9
Q
advantage of parenteral route
A
more rapid and predictable absorption, useful in unconscious or vomiting person
10
Q
disadvantage of parenteral admin
A
needs to be aseptic, could cause pain/irritation, can’t give insoluble drugs via IV, much harder to “take back” a dose once given
11
Q
what sort of drug will more readily cross plasma membranes
A
small, non-ionized, lipid soluble drugs
12
Q
when a drug is absorbed via GI tract what does it go through before entering the systemic circulation
A
portal circulation aka first pass hepatic metabolism
13
Q
what happens if a drug is rapidly metabolized in the liver
A
a smaller amount of the drug in the original unchanged state will reach the target tissues
14
Q
what kind of drug can the kidney not efficiently eliminate
A
lipid soluble, so they are reabsorbed from kidney back into systemic circulation
15
Q
Phase I drug metabolism involves
A
converting lipid soluble molecules into water soluble by introducing or unmasking a polar group (-OH or -NH2)
16
Q
Phase I reaction are most frequently catalyzed by
A
cytochrome P450
17
Q
Phase II reactions consist of
A
conjugation, wherein an endogenous polar group is added to a drug molecule (ex: glucuronic acid, sulfuric acid, acetic acid, amino acid) so that it can be excreted from the kidney
18
Q
bioavailability is
A
fraction of administered drug that reaches systemic circulation in an unchanged form…(if 100 mg of a drug is taken orally and 70 mg of the drug is absorbed unchanged, then the bioavailability of that drug is 70%)
19
Q
half life is
A
the amount of time required for the plasma concentration of a drug to decrease by 50% after discontinuation of a drug
20
Q
a loading dose is
A
an initial dose of drug that is higher then subsequent doses for the purpose of rapidly achieving therapeutic drug concentrations in the serum.
21
Q
efficacy refers to
A
the degree to which a drug is able to induce maximal therapeutic effects. Efficacy is a term often used to compare drugs of different classes.
22
Q
potency is
A
the amount of drug required to produce 50% of the maximal response that the drug is capable of inducing. Potency is a term more frequently used to compare drugs of a similar class.
23
Q
the EC50 or effective concentration 50 is
A
the concentration or dosage of an agent which induces a specified clinical effect in 50% of the subjects to which the drug has been administered.
24
Q
LD50 or lethal dose 50 is
A
the concentration or dosage of an agent or drug which causes death in 50% of the subjects to which that agent or drug has been administered.
25
therapeutic index (TI) is
a ratio of the dose of a drug that produces toxicity relative to the dose of the same drug that produces a clinically desired response. Looked at as an equation, this would be T.I. = LD50 / EC50...thus a measure of the drug's safety. A large value indicates that there is a wide margin between an effective dose and a toxic dose.
26
competitive antagonists
interact with the receptors at the same site as the agonist and thus compete for binding with the agonist. (May be reversible or irreversible)
27
noncompetitive antagonists
bind to a site other then the agonist binding domains. (Effects generally irreversible)
28
physiologic antagonism
refers to two agonists in unrelated reactions which cause opposite effects.
29
neutral antagonism
refers to a process in which two drugs bind to one another which serves to inactivate or partial inactivate each of the drugs.
30
CI drug
no approved medical use
31
CII drug
high potential for abuse
32
CIII drug
moderate potential for abuse
33
CIV drug
low potential for abuse
34
X drug
contraindicated in pregnancy
35
q
every
36
qH
every hour
37
qAM
every morning
38
qPM
every evening
39
qHS
every bedtime
40
qD
every day
41
qOD
every other day
42
BID
two times a day
43
TID
three times a day
44
QID
four times a day
45
_xD
_ times a day
46
qWK
every week
47
qMO
every month
48
PRN
as needed
49
Stage 2 HTN
160-179/100-109
50
Stage 3 HTN
>180/110
51
Most common cause of chronic renal disease
HTN
52
Primary HTN etiology
unknown
53
What catalyzes angiotensinogen to angiotensin I
renin, a proteolytic enzyme formed in the granules of juxtaglomerular cells
54
Angiotensin I goes to Angiotensin II by being cleaved by
ACE (angiotensin converting enzyme) which is found mostly in the lungs but also the kidneys and brain and elsewhere
55
most potent vasoconstrictor produced by the body
angiotensin II
56
in response to HTN the smooth muscle cells surrounding and within arterioles develop
hypertrophy and hyperplasia which causes artery lumen size to decrease
57
most common side effect of hypertensive drugs is
hypotension
58
two/three classifications of diuretics
potassium wasting, potassium sparing, combination of the two
59
how do thiazide diuretics work
increase sodium and water excretion into urine by inhibiting sodium and chloride reabsorption in the cortical thick ascending limb and early distal tubule
60
side effect on minerals when taking thiazide diuretics
can cause calcium and uric acid to be reabsorbed by proximal tubule in increased amounts...so serum levels of calcium and uric acid rise
61
thiazide diuretics are best used for
initial treatment of mild HTN, particularly in the setting of chronic edema
62
how are thiazide diuretics delivered
oral route
63
onset of action for thiazide diuretics
1 hour
64
thiazide diuretics are often used in conjunction with
other HTN meds like beta blockers and ACE inhibitors
65
side effects of thiazide diuretics
hypotension, weakness, dizziness, hyponatremia, hypokalemia, hypercalcemia, hyperuricemia, glucose intolerance, hypercholesterolemia, and hypertriglyceridemia
66
Primary thiazide diuretic
hydrochlorthiazide (HCTZ)/hydrodiuril
67
indication for hydrochlorthiazide/hydrodiuril
HTN, chronic edema, hypocalcemia when due to excessive urinary loss of calcium
68
MOA of hydrochlorthiazide/hydrodiuril
inhibition of sodium and chloride reabsorption in ascending limb and distal tubule
69
Char of hydrochlorthiazide/hydrodiuril
PO, rapid absorption
70
dose for hydrochlorthiazide/hydrodiuril
25-100 mg per day in single or divided doses
71
what supplement is generally recommended when taking hydrochlorthiazide/hydrodiuril
potassium
72
hydrochlorthiazide/hydrodiuril should not be used by
patients with a sulfa allergy, they contain a sulfonamide moiety
73
thiazide diuretics are not effective in patients with
renal failure
74
main loop diuretic
furosemide/lasix
75
what do loop diuretics do
inhibit chloride reabsorption in the ascending loop of Henle by blocking the Na+/K+/Cl- co-transporter system
76
stronger diuretic: loop diuretics or thiazide
Milligram for milligram, thiazides have a lesser diuretic action than the loop diuretics...This is because the loop of Henle plays a greater role in sodium resorption than does the thick ascending limb and distal tubule
77
what happens at the thick ascending limb
thick ascending limb is a major site of calcium and magnesium reabsorption, processes which are dependent on normal sodium and chloride reabsorption
78
loop diuretics can increase the loss of
sodium, potassium, calcium, and magnesium
79
the use of a loop diuretic can potentially cause electrolyte abnormalities such as
hyponatremia, hypokalemia, hyperglycemia (presumed due to impaired insulin release), hypocalcemia, hypomagnesemia and hyperuricemia
80
initial onset of action for loop diuretics
20-30 min (half life of 1-1.5 hours)
81
loop diuretics are the prefered diuretic in patients with
renal disease (low GFR) and in hypertensive emergencies
82
loop diuretics are useful in conditions that are refractory to less potent diuretic, for example
CHF, renal insufficiency, and nephrotic syndrome...can also be used to treat hypercalcemia since they increase calcium excretion
83
who should loop diuretics be used with caution in
patients who are more likely to be susceptible to volume contraction (hypovolemia) and patients prone to dehydration
84
indication for furosemide/lasix
HTN, acute or chronic edema, hypercalcemia. Preferred diuretic in hypertensive patients with renal disease.
85
MOA of furosemide/lasix
inhibition of sodium and chloride reabsorption in the loop of henle
86
char of furosemide/lasix
PO/IV rapid absorption
87
side effects of furosemide/lasix
may potentiate orthostatic hypotension, contains a sulfonamide moiety and shouldn't be used with patients who have sulfonamide allergies. Not effective in patients with renal failure.
88
average dose for potassium replacement
10 mEq which is equal to 750 mg of microencapsulated potassium chloride, USP.
89
what do potassium sparing diuretics do
increase sodium excretion and inhibit potassium secretion in the distal convoluted tubule
90
examples of disease states the potassium sparing diuretics should not be used with
severe renal insufficiency, poorly controlled DM, and multiple myeloma
91
drugs that can cause hyperkalemia
ACE inhibitors and Angiotensin II receptor blockers
92
primary potassium sparing diuretic
spironolactone/aldactone
93
indication for spironolactone/aldactone
HTN, chronic edema, hypercalcemia. May be used in patients with renal disease but not anuric patients. Used to treat hyperaldosteronism. Has anti-androgenic properties and is thus used to treat hirsutism and PCOS
94
MOA of spironolactone/aldactone
inhibits sodium and chloride reabsorption while promoting potassium reabsorption in the distal tubule...also a direct antagonist of aldosterone so it helps increase urinary sodium loss and reduce vascular volume
95
Char of spironolactone/aldactone
takes up to 1 to 2 days before increased diuresis (half life 1-1.5). Can't be given with other classes of diuretics. Not effective in patients with renal failure.
96
Side effects of spironolactone/aldactone
hyperkalemia, avoid with patients on potassium supplementation/ACE inhibitors/ARBs
97
beta blockers reduce blood pressure by
reducing adrenergic receptors in the heart (B1) thereby decreasing cardiac output. Non-selective beta blockers also diminish peripheral vasoconstriction by reducing adrenergic input at B-2 receptor sites on smooth muscle surrounding the peripheral vasculature.
98
prototype B-blocker
propranolol/inderal
99
propranolol acts at
B-1 and B-2 receptor sites
100
beta blocker atenolol/tenormin acts at
B-1 receptors (selective)
101
selective B-1 receptor blockage helps to avoid
potential for bronchospasm that may result when B-2 receptors are blocked
102
even cardioselective B-blockers are contraindicated in patients with
severe asthma or COPD who are known to have a prominent bronchospastic component that is sensitive to beta blockade
103
disadvantage of B-blockers include
high incidence of adverse CNS affects, sexual dysfunction in men/women, and bradycardia
104
contraindications of beta blockers include
certain cardiac conduction abnormalities, severe asthma, and severe COPD
105
abrupt withdrawal of beta blockers can result in
rebound HTN and/or rebound tachycardia, probably due to up-regulation of beta receptors during treatment...can result in MI or stroke
106
overdose of a beta blocker can result in
bradycardia and heart block
107
treatment of choice to reverse bradycardic effects of a beta blocker is
the hormone glucagon
108
MOA for glucagon to reverse B-blocker
increase of cAMP in myocardium, effectively bypassing the B-adrenergic second messenger system
109
class of propranolol/inderal
non-selective beta blocker (B-1 and 2)
110
indication of propranolol/inderal
HTN, angina and acute MI, tachyarrhythmias, migraine headache prophylaxis, essential tremors
111
MOA of propranolol/inderal
adrenergic blockage at beta receptors
112
Char of propranolol/inderal
PO, IV. There's also oral time-released form that is longer acting i.e. Inderal LA.
113
Side effect of propranolol/inderal
may potentiate orthostatic hypotension especially if mixed with alcohol or narcotic analgesics. Weakness, fatigue, depression, sexual dysfunction.
114
Atenolol/tenormin class
Beta 1 blocker (cardioselective)
115
indication of atenolol/tenormin
HTN, angina and acute MI, and several forms of tachyarrhythmia. Atenolol is indicated in the management of hemodynamically stable patients with definite or suspected acute MI to reduce cardiovascular mortality.
116
MOA of atenolol/tenormin
adrenergic blockage at the beta 1 receptor sites
117
Char of atenolol/tenormin
PO, IV. Peak blood levels are usually reached between 2 and 4 hours after ingestion. Follow pulse rate.
118
side effects of atenolol/tenormin
cardioselective effect is not absolute and at higher doses, blockage of beta 2 receptors can occur. Contraindicated in certain arrhythmias and heart blocks. Use cautiously in combo with calcium channel blockers.
119
first line treatment of HTN by the books
diuretics
120
first line treatment of HTN in conventional clinical practice
ACE inhibitors and calcium channel blockers
121
two ways asthma meds work
relax bronchial smooth muscle, reduce inflammation
122
sympathetic (adrenergic) tone causes ___ in the lungs
bronchodilation
123
parasympathetic (cholinergic) tone causes ___ in the lungs
bronchoconstriction
124
treatment for acute asthmatic attacks that are unresponsive to other medications
epinephrine (adrenalin)
125
how does epinephrine work
non-selective adrenergic agonist that binds to alpha, beta-1, and beta-2 receptors. Causes cardiac stimulation via beta-1 receptors resulting in possible tachycardia, palpitations, and potential arrhythmias.
126
class of epinephrine
adrenergic agonist
127
indication of epinephrine
emergent treatment of asthma, status asthmaticus, anaphylaxis
128
MOA of epinephrine
Powerful β-2 agonist activity results in increased cAMP. Increased cAMP causes immediate relaxation of bronchial smooth muscle cells and resultant bronchodilation
129
Char of epinephrine
SQ, IV, IM, inhalation, endotracheal tube administration. Rapid onset of action but brief duration of action.
130
what is primatene mist
OTC preparation containing a very low dose of epinephrine
131
side effects of epinephrine
tachycardia, increased cardiac demand, anxiety, dry mouth (alpha 1 effect) and hyperglycemia
132
class of albuterol/ventolin, proventil
beta 2 agonist
133
indication of albuterol/ventolin, proventil
treatment of acute, uncomplicated asthma symptoms
134
MOA of albuterol/ventolin, proventil
Bronchodilation via β2 adrenergic receptor stimulation, increased cAMP levels and resultant bronchial smooth muscle relaxation
135
Char of albuterol/ventolin, proventil
Inhaled route results in onset of action in ~15 minutes with a duration of action of 3-4 hours. PO route has onset of action of ~ 30 minutes and a duration of action of 4-8 hours. Average dose is 2 puffs orally, 3 to 4 times a day
136
side effects of albuterol/ventolin, proventil
Although promoted as a β-2 selective agonist, β-1 agonist activity is also reported with predictable potential side effects of tachycardia, palpitations, anxiety, etc. Beta blockers inhibit activity. No anti-inflammatory effects.
137
class of salmeterol/severent
long acting beta 2 agonist
138
indication of salmeterol/severent
chronic treatment of asthma or bronchospasm. Not for treatment of acute asthma.
139
MOA of salmeterol/severent
bronchodilation via Beta-2 adrenergic receptor stimulation
140
Char of salmeterol/severent
inhaled only. Onset of action about 20-30 min with a duration of action of 12 hours. Usually dosed twice daily.
141
Side effects of salmeterol/severent
headache, cough,. Beta blockers inhibit activity.
142
how do anticholinergic drugs work
competitive antagonists at muscarinic acetylcholine receptor sites. Antagonism results in unopposed sympathetic tone in the airways with resultant smooth muscle relaxation and bronchodilation.
143
when are anticholinergic drugs typically indicated
generally not indicated for acute asthma attacks but rather for maintenance therapy in asthma patients who cannot tolerate treatment with a beta agonist
144
primary anticholinergic drug
ipratropium/atrovent
145
what do leukotriene inhibitors do
antagonism of leukotriene receptor sites in bronchial wall smooth muscle
146
class of zafirlukast/accolate
leukotriene receptor antagonist
147
indication of zafirlukast/accolate
prophylaxis and treatment of chronic asthma
148
MOA of zafirlukast/accolate
Competitive antagonism of leukotriene D4 and E4 receptors result in inhibition of bronchoconstriction and inflammation. Not indicated for reversal of bronchospasm in acute asthma attacks
149
Char of zafirlukast/accolate
PO. Well absorbed. Peak levels in 3 hours. Inhibits cytochrome P450 enzymes. Effects are somewhat similar to those expected with Cromolyn
150
Side effects of zafirlukast/accolate
headache, GI distress, diarrhea, older patients may have increased incidence of respiratory infections
151
how do corticosteroids work
inhibition of phospholipase A2 blocks release of arachadonic acid, the precursor of the prostaglandins and leukotrienes from membrane bound phospholipids. Histamine release and kinin activity is also suppressed by glucocorticoids.
152
side effects of glucocorticoides include
reduced resistance to infections, hyperglycemia, severe bone loss, avascular necrosis, cataracts, myopathy, thinning of skin, diminished wound healing, insomnia and mental status changes
153
primary inhaled steroid
beclomethasone/beclovent, vanceril
154
class of beclomethasone/beclovent
corticosteroid
155
indication of beclomethasone/beclovent
asthma not controlled by sympathomimetics (bronchodilators) alone
156
MOA of beclomethasone/beclovent
decreased inflammation and edema in the respiratory tract via reduction in number and activity of macrophages, eosinophils, and T-lymphocytes. Mucosal edema reversed by decreasing the permeability of capillaries and inhibiting the release of leukotrienes. No direct effect on airway smooth muscle.
157
Char of beclomethasone/becolvent
Similar to the beta adrenergic drugs, the inhaled route of steroids allows for fewer systemic side effects. However, it is also common for ~90% of total amount inhaled to be deposited in mouth and larynx and only ~10% directly deposited in airways. Placement of “spacer” may allow for improved delivery
158
Side effects of beclomethasone/beclovent
Inhaled steroids generally have fewer side effects then P.O. steroids. Oropharyngeal yeast infection or thrush can occur. Rinsing mouth after inhaler use can help to reduce incidence of thrush. The potential for adrenal suppression is small but does exist
159
Class of prednisone/deltasone
corticosteroid
160
indication for prednisone/deltasone
COPD, worsening asthma
161
MOA of prednisone/deltasone
decrease inflammation and edema in respiratory tract
162
Char of prednisone/deltasone
PO, (IV and IM corticosteroids are also available). Steroids must be considered as adjunct therapy and discontinued as soon as possible. Dose 10 to 100 mg 1 to 2 times daily
163
side effects of prednisone/deltasone
Salt and water retention, fat gain and redistribution, hyperglycemia and diabetes, osteoporosis and pathologic fractures, adrenal suppression. Abrupt withdrawal of prednisone or other drugs with corticosteroid properties may result in severe and potentially life threatening hypofunction of the adrenal glands, also known as Addisonian crisis.
164
What's significant about theophylline/theo-dur
bad TI, lethal dose is not far from effective dose
165
class of theophylline/theo-dur
xanthine or methylxanthine bronchodilators
166
MOA of theophylline/theo-dur
no exactly known but one mechanism is the inhibition of phosphodiesterase, the enzyme which breaks down cAMP
167
two narcotic analgesic antitussives
codeine and hydrocodone...decrease sensitivity of response in cough centers that exist within CNS
168
class of codeine
narcotic analgesic and cough suppressant
169
indication for codeine
pain relief, cough suppression
170
MOA of codeine
suppresses the sensitivity of CNS cough centers in the medulla
171
Char of codeine
PO. Onset of action generally within 30 to 60 min. Often formulated with an antihistamine in a syrup. Usual dose 1 to 2 tsp every 4-6 hours.
172
Side effects of codeine
drowsiness, constipation, GI upset, potential for drug dependence
173
Class of dextromethorphan
synthetic derivative of morphine
174
indication of dextromethorphan
cough suppression
175
MOA of dextromethorphan
suppresses the sensitivity of CNS cough centers
176
Char of dextromethorphan
PO. Onset of action 30-60 minutes. No analgesic or addictive potential. Less constipating then the narcotic based antitussives. Often formulated with an antihistamine in a syrup. Usual dose 1 to 2 tsp every 4 to 6 hours.
177
class of diphenhydramine/benadryl
antihistamine
178
indication of diphenhydramine/benadryl
allergic rhinitis and conjunctivitis, urticaria, pruritis, often to induce sleep
179
MOA of diphenhydramine/benadryl
H1 receptor site blockage. The production and release of histamine is not blocked.
180
Char of diphenhydramine/benadryl
PO, dose 25-100 mg every 6-8 hours. Readily crosses the blood brain barrier.
181
side effects of diphenhydramine/benadryl
Variable degrees of sedation (recall that this drug class exhibits ready passage through the BBB), drying and thickening of secretions (which may actually worsen symptoms of asthma or sinusitis) and possible urinary retention...Think of this side effect profile whenever a pharmacologic agent is described as being anti-cholinergic.
182
primary non-sedating antihistamine
loratadine/claritin
183
class of loratadine/claritin
non-sedating antihistamine
184
indication of loratadine/claritin
seasonal allergic rhinitis, hay fevere
185
MOA of loratadine/claritin
H1 receptor antagonist
186
Char of loratadine/claritin
Does not readily cross the BBB, thus little to no sedation. Usual dose is once a day.
187
Side effects of loratadine/claritin
drying of secretions. Dry mouth is common.
188
alpha agonist nasal spray (decongestants) often significant
rebound effects...so there is a high incidence of "dependence" (rhinitis medicosum)
189
Smoking cessation meds in order of least to most effective
gum, lozenges, transdermal patches, oral, nasal spray
190
Mechanisms of varenicline/chantix
partial agonist of alpha 4/beta 2 nicotinic acetylcholine receptor sites
191
side effects of varenicline/chantix
increasing reports of neuro-psychiatric symptoms that range from nightmares or insomnia to depression and suicidal ideations to increased agitation and rage
192
stimulation of alpha adrenergic receptors in the peripheral vasculature results in
vascoconstriction
193
blockade of alpha blockers results in
reduced sympathetic tone, thereby causing vasodilation and decreased peripheral resistance
194
alpha blockers also block alpha 1 receptors in the smooth muscle of the bladder neck and prostate so they help improve urine flow in people with
BPH
195
primary alpha blocker
prazosin/minipress (alpha 1)
196
class of prazosin/minipress
alpha 1 adrenergic blocker
197
indication of prazosin/minipress
HTN, BPH
198
MOA of prazosin/minipress
blockage of alpha 1 receptors
199
Char of prazosin/minipress
PO. Vasodilation. Can relax tone in bladder neck.
200
Side effects of prazosin/minipress
dizziness, H/A, orthostatic hypotension, impotency
201
calcium channel blockers cause
dilation of both cardiac and peripheral vessels (mainly arterioles)
202
calcium channel blockers are used for
treatment of HTN, angina, and cariac arrhythmias. Also used as prophylaxis of migraine headache and for Raynaud's syndrome
203
3 main classes of calcium channel blockers
Benzothiazepine, Diphenyl alklamine, Dihydropyridine
204
Most common side effects of calcium channel blockers include
hypotension, dizziness, headache, and flushing of skin
205
calcium channel blockers should be used with more caution in patients with
bradycardia or severe CHF
206
class of verapamil/isopten
calcium channel blocker
207
indication of verapamil/isopten
HTN, angina--especially vasospastic angina, CHF
208
MOA of verapamil/isopten
blocks calcium influx with resultant peripheral vasodilation and improved myocardial tone
209
Char of verapamil/isopten
PO, slow onset of action. Effects of peripheral vasodilation often useful in reducing both preload and afterload
210
side effects of verapamil/isopten
Flushing, H/A, hypotension. Caution when using concurrently with beta blockers in terms of potential increased risk for bradycardia and possible arrhythmias. Upon the discontinuation of a calcium channel blocker, there is generally less risk for rebound hypertension then when discontinuing a beta blocker.
211
long term use of calcium channel blockers is associated with increased risk for
developing breast cancer
212
ACE inhibitors reduce BP by
interfering with the generation of Angiotensin II from Angiotensin I...also inhibit the degradation of bradykinins, allowing for another mechanism by which peripheral vascular resistance can be reduced
213
ACE inhibitors are excellent first line agent in hypertensive patients with
congestive heart failure as well as hypertensive patients with diabetes
214
what drug is considered least likely of the antihypertensive drugs to cause sexual dysfunction in males
ACE inhibitors
215
How do ACE inhibitors affect serum lipids, glucose or uric acid levels
ACE inhibitors do not adversely affect
216
ACE inhibitors can potentially increase serum
potassium
217
ACE inhibitors are often the drug of choice in treating HTN patients with
diabetes...demonstrated an ability to slow development of diabetic nephropathy
218
With ACE inhibitors, avoid concurrent use of
potassium sparing diuretic...but potassium wasting diuretics are quite commonly used in conjunction
219
All ACE inhibitors have potentially adverse side effect of
dry irritating cough
220
ACE inhibitors and pregnancy
contraindicated in pregnancy due to fetal pulmonary and developmental abnormalities
221
Rare potential adverse effect of all ACE inhibitors that can be life threatening
Angioedema, life threatening when it involves the tongue and oropharyngeal area
222
Primary ACE inhibitor
Lisinopril/Prinivil or Zestril
223
Class of Lisinopril/Prinivil or Zestril
ACE inhibitor
224
indication of
HTN, shown to improve mortality and morbidity in post-MI patients
225
MOA of Lisinopril/Prinivil or Zestril
Blocks conversion of angiotensin I to angiotensin II, resulting in significant decrease in peripheral vascoconstriction
226
Char. of Lisinopril/Prinivil or Zestril
often used concurrently with a potassium wasting diuretic
227
Side effects of Lisinopril/Prinivil or Zestril
hypotension, potential hyperkalemia, contraindicated in pregnancy (category X). May cause dry, irritating cough. May cause severe and life threatening angioedema in susceptible patients.
228
Angiotensin II receptor blockers are an excellent first line agent in HTN patients with
CHF as well as HTN patients with DM
229
Do Angiotensin II receptor blockers block the degradation of bradykinins?
No
230
Do Angiotensin II receptor blockers cause cough and angioedema?
Yes, although their potential to do so is less than ACEI
231
Do Angiotensin II receptor blockers cause hyperkalemia?
Yes
232
Precautions for use of ACE inhibitors
patients with hyperkalemia, hypovolemia, or severe renovascular disease. Strictly contraindicated in pregnant patient (category X)
233
primary Angiotensin II receptor blocker
Losartan/Cozaar
234
Class of Losartan/Cozaar
Angiotensin II receptor antagonist
235
indication of Losartan/Cozaar
HTN, diabetic nephropathy with proteinuria
236
MOA of Losartan/Cozaar
blocks the effects of Angiotensin II resulting in significant decrease in peripheral vasoconstriction
237
Char. of Losartan/Cozaar
PO, often used along with a non-potassium sparing diuretic
238
side effects of Losartan/Cozaar
hypotension, potential hyperkalemia, contraindicated in pregnancy. Persistent dry cough. Angioedema
239
how do centrally acting alpha agonists work
stimulate the presynaptic alpha 2-adrenergic receptors in the CNS
240
side effects of centrally acting alpha agonists
marked sedation, fatigue, orthostatic hypotension
241
how do direct vasodilators work
cause arterial dilation by opening K+ channels in vascular smooth muscle cells
242
example of a direct vasodilator
Minoxidil/Loniten
243
Minoxidil is generally reserved for
severe hypertension, resistant to previous antihypertensive treatment attempts
244
What is the more potent direct vasodilator: Minoxidil or Hydralazine?
Minoxidil is more potent than Hydralazine but it is associated with more adverse effects, including potential for marked sodium and water retention and hirsutism
245
Unique side effect of minoxidil
hirsuitism
246
hydralazine is generally reserved for
severe HTN resistant to previous antihypertensive treatment attempts
247
Hydralazine can result in the side effect known as
drug induced lupus syndrome
248
first drug FDA approved in new antihypertensive drug class known as direct renin inhibitors
Aliskiren (Tekturna)
249
side effects of Aliskiren (Tekturna)
hypotension, headache, diarrhea, hyperkalemia, and angioedema
250
principal action of IV nitroglycerin
vasodilation of both arteries and veins (veins more so)
251
indication for IV nitroglycerin
manage HTN during and after coronary bypass, heart failure, acute MI, unstable angina pectoris and acute pulmonary edema
252
What is IV sodium nitroprusside converted to in the body?
nitric oxide
253
MOA of IV Labetalol
alpha-1 and beta adrenergic blocker
254
the oral form of labetalol is indicated in
treatment of pregnancy induced HTN
255
Prinzmetal angina occurs at
rest, rather than exertion
256
three main classes of drugs that have proven very effective in treating patients with stable angina pectoris
nitrates, beta blockers, calcium channel blockers
257
Nitric oxide, derived from nitrates, activate ___
guanyl cyclase and increase the intracellular cyclic GMP which results in vascular smooth muscle relaxation
258
two main classes of nitrate drugs
nitroglycerin (ntg)/nitrostat and isosorbide dinitrate/isordil
259
class of nitroglycerin/nitrostat
nitrate vasodilator
260
indications of nitroglycerin/nitrostat
all forms of angina. may be used for acute relief of angina or prophylaxis of angina prior to increased exertional activtiy
261
MOA of nitroglycerin/nitrostat
immediate vasodilation via production of nitric oxide. dilation of myocardial arteries increases blood supply to the myocardium. preload is reduced by reducing peripheral venous tone.
262
Char. of nitroglycerin/nitrostat
SL, oral spray, topical paste, transdermal patch and I.V. routes. SL doses of reach peak levels in 1 to 2 minutes and have a duration of 30 to 60 minutes. Topical paste has onset of action in 30 to 60 minutes and a duration of 2 to 12 hours. Transdermal NTG reaches peak activity in 30 to 60 minutes and has a duration of action of 24 hours. IV NTG has an onset of action in 1 to 2 minutes and has a duration of action of 3 to 5 minutes.
263
side effects of nitroglycerin/nitrostat
Headache, hypotension, rebound tachycardia. Alcohol, antihypertensives and vasodilators increase the risk of orthostatic hypotension. Use with Silendafil (Viagra) is contraindicated due to potential for causing severe hypotension.
264
class of isosorbide dinitrate/isordil
long acting nitrate vasodilator
265
indication of isosorbide dinitrate/isordil
angina, prophylaxis of angina
266
MOA of isosorbide dinitrate/isordil
similar to NTG
267
Char. of isosorbide dinitrate/isordil
SL, Oral. SL has onset of action by 5 min. with duration of action of 1 to 4 hours. Oral form has onset of action in 30 minutes with duration of 4 to 6 hours, up to 8 hours with sustained released forms. Not readily metabolized by the liver. Lower potency than nitroglycerin in relaxing vascular smooth muscle.
268
Side effects of isosorbide dinitrate/isordil
headache, hypotension, rebound tachycardia. Concurrent use of alcohol, antihypertensives and vasodilators increase the risk of orthostatic hypotension. Concurrent use of Silendafil (viagra) and Isosorbide is contraindicated due to the potential for severe hypotension.
269
beta blockers diminish cardiac oxygen demand by
decreasing both cardiac contractility and cardiac rate
270
the occupation of cardiac beta 1 receptor sites by a beta blocking agent also acts to protect the heart from full effects of
sympathetic (nor-epinephrine and epinephrine) stimulation
271
in patients with acute myocardial infarction, beta blockers have been shown to
decrease the size of the infarct
272
the treatment of choice to reverse the bradycardic effects of a beta blocker is
hormone glucagon...likely mechanism is increase in cAMP in the myocardium, effectively bypassing the Beta-adrenergic second messenger system
273
Class of propranolol/inderal
non-selective beta blocker
274
indication of propranolol/inderal
angina, status-post myocardial infarction, hypertension, panic attacks, migraine headache
275
MOA of propranolol/inderal
blocks adrenergic stimulation which serves to decrease heart rate and myocardial oxygen demand and also decreases renin release
276
Char. of propranolol/inderal
PO, IV non selective beta blockade with potential for bronchoconstriction via antagonism of Beta 2 receptors in bronchi
277
side effects of propranolol
Bronchoconstriction, hypotension, bradycardia, fatigue, impotence. Abrupt discontinuation may cause rebound hypertension and tachycardia with subsequent increase in myocardial oxygen demand. Abrupt discontinuation increases the risk of arrythmias, stroke, angina and M.I. Can increase the effects of calcium channel blockers.
278
class of atenolol/tenormin
selective beta blocker
279
indication of atenolol/tenormin
angina, HTN, MI
280
MOA of atenolol/tenormin
decrease heart rate and myocardial oxygen demand by selective B1 adrenergic blockade
281
Char. of atenolol/tenormin
PO and IV, PO decreased risk bronchoconstriction relative to non-selective beta blockers
282
Side effects of atenolol/tenormin
similar to propranolol with less risk for bronchoconstriction
283
treatment of choice to reverse the symptomatic effects of bradycardia of a calcium channel blocker is
calcium gluconate...but glucagon can be given if calcium gluconate increases pulse rate
284
class of amlodopine/norvasc
calcium channel blocker
285
indication of amlodopine/norvasc
angina--especially variant or vasospastic angina, HTN
286
MOA of amlodopine/norvasc
blocks calcium influx with resultant vasodilation of ardiac and peripheral arteries. diminishes sympathetic induced coronary artery spasm
287
Char of amlodopine/norvasc
PO, slow onset of action, 3 to 6 hours
288
side effects of amlodopine/norvasc
flushing, headache, hypotension. calcium channel blockers can act synergistically with beta blockers with a resultant increased risk for hypotension and bradycardia
289
what do you do with someone with unstable angina
administer MONA = morphine, oxygen, nitrate, aspirin
290
standard analgesic in cases of unstable angina and/or myocardial infarction
morphine sulfate via IV
291
how do you reverse morphine
Naloxone
292
class of morphine sulfate
analgesic
293
indication of morphine sulfate
pain relief, especially in setting of unstable angina or MI
294
MOA of morphine sulfate
opiate receptor agonist
295
Char of morphine sulfate
PO, IV, IM, SQ, PR. Mild vasodilator. Potent analgesis. Anxiolytic.
296
Side effects of Morphine Sulfate
Potential for respiratory depression must be monitored. Potential for severe hypotension.
297
class of aspirin/ASA
salicylate with anti-inflammatory analgesic and antipyretic properties
298
indication for aspirin/ASA
Reduces the risk of M.I. in patients with unstable angina or prior infarction. Reduces risk of recurrent transient ischemic attacks and stroke.
299
MOA for aspirin/ASA
Irreversibly inhibits cyclooxgenase enzyme. Inhibition of cyclooxgenase prevents the formation of thromboxane A2 and prostaglandins with resultant diminished platelet aggregation.
300
Char of aspirin/ASA
P.O., adult dose - 325 mg, children’s dose - 81 mg. Aspirin is well absorbed in upper small intestine, Metabolized in liver
301
side effects of aspirin/ASA
G.I. ulceration, bleeding, salicylism with hyperventilation, tinnitus, dizziness, nausea and vomiting. Markedly increased risk for the development of Reye’s syndrome in children with fevers due to viral conditions such as mumps or chickenpox.
302
ADP receptor antagonists can be used in patients who are
intolerant or allergic to aspirin
303
class of Clopidogrel/ Plavix
platelet aggregation inhibitor
304
Indication of Clopidogrel/ Plavix
reduces thrombotic events. Shown to decrease incidence of MI and stroke
305
MOA of Clopidogrel/ Plavix
ADP receptor blockade results in diminished platelet aggregation
306
Char. of Clopidogrel/ Plavix
generally preferred over Ticlopidine (Ticlid) because it more rapidly inhibits platelets and appears to have a more favorable safety profile
307
side effects of Clopidogrel/ Plavix
Bleeding, nausea, headache, neutropenia. Contraindicated in patients with active bleeding i.e. a bleeding peptic ulcer. The anti-platelet activity of these drugs is considered to be “irreversible”, that is, the effect generally lasts for the life of the affected platelet. Use cautiously, if at all, when a patient is taking Coumadin.
308
what do Glycoprotein IIB/IIIA inhibitors do
prevent the binding of fibrinogen, thereby blocking platelet aggregation.
309
class of Abciximab/ ReoPro
glycoprotein IIB/IIIA inhibitor
310
indcation of Abciximab/ ReoPro
Reduces risk of M.I. Abciximab has been approved for use in elective/urgent/emergent percutaneous coronary intervention.
311
MOA of Abciximab/ReoPro
Inhibition of Glycoprotein IIB/IIIA receptor sites on platelets prevents the binding of fibrinogen and Von Willebrand’s factor to activated platelets, resulting in decreased platelet aggregation.
312
Char. of Abciximab/ReoPro
IV administration only. Abciximab is a monoclonal antibody fragment. The platelet anti-aggregation effects from a single dose will last for 24 – 48 hours.
313
Side effects of Abciximab/ReoPro
Increased bleeding, strictly contraindicated in patients with active internal bleeding, a history of intracranial hemorrhage, head trauma or history of stroke within the previous 30 days.
314
how does regular weight heparin act as an anti-coagulant
Regular weight heparin acts as an anti-coagulant by binding to antithrombin III. The heparin-antithrombin III complex then binds to and inactivates activated factor X (Xa) and factor II (thrombin).
Heparin ultimately acts to prevent conversion of fibrinogen to fibrin.
Heparin does not actively lyse clots but is able to inhibit further thrombogenesis.
315
How is Heparin given
parenterally--IV or SQ
316
Indications for Heparin
Heparin has been widely used an anticoagulant for unstable angina, acute M.I, atrial fibrillation and post-P.E. due to D.V.T., however in this country, low-molecular weight heparin has largely replaced regular weight heparin because of it’s better side effect profile.
317
What reverses the effects of heparin
Protamine sulfate
318
how does low molecular weight heparin act
directly inactivates factor X (Xa) in the clotting cascade...proven to be as effect as regular weight Heparin but with fewer reported side effects
319
low molecular weight heparin has been show to reduce
cardiac ischemic events and death by as much as 15% in patients with unstable angina
320
class of Enoxaparin/ Lovenox
low molecular weight heparin
321
indication of Enoxaparin/ Lovenox
unstable angina, acute MI, prophylaxis and treatment of DVT and PE
322
MOA of Enoxaparin/ Lovenox
binds to and inactivates activated factor X (Xa)
323
Char of Enoxaparin/ Lovenox
therapeutic anticoagulant effects are notes when clotting time is 2 to 2.5 times longer than normal clotting time
Char: SQ/IV , Rapid onset of action. Anticoagulant effects of low molecular weight heparin may be reversed with Protamine sulfate, a heparin antagonist.
Heparin and low dose heparin can be administered to pregnant women.
Labs: Follow serum levels of clotting factor Xa, aPTT, CBC and platelet count.
324
side effects of Enoxaparin/Lovenox
Hemorrhage, caution in patients with liver disease, bleeding disorders such as G.I. bleed. Discontinue if sign of bleeding are noted. Life threatening thrombocytopenia - known as Heparin induced thrombocytopenia (HIT) syndrome can occur. Discontinue Enoxaprin if the patient’s platelet count falls below 100,000/mm3.
325
Class of Warfarin/Coumadin
oral anticoagulant
326
indication of Warfarin/Coumadin
Prophylaxis and treatment of DVT, PE and thromboembolic events associated with atrial fibrillation and/ or cardiac valve replacement.
327
MOA of Warfarin/Coumadin
Antagonizes vitamin K. This interferes with the synthesis of vitamin K dependent clotting factors (factors II, VII, IX, and X).
328
Char. of Warfarin/Coumadin
PO only. Very well absorbed. Metabolized by liver, half life approx. 37 hours
329
Side effects of Warfarin/Coumadin
Bleeding. Check Protime (PT) or INR (International Normalized Ratio) to maintain optimal blood levels.
330
Anti-coagulant effects of Coumadin may be reversed with
Vitamin K, often administered IV in an emergent situation
331
Coumadin should not be used by
Pregnant women--category X
332
class of Rivaroxaban/ Xarelto
anticoagulant
333
indication of Rivaroxaban/ Xarelto
Prophylaxis of deep vein thrombosis which may lead to pulmonary embolism in adults undergoing hip and knee replacement surgery as well as stroke prophylaxis in patients with non-valvular disease induced atrial fibrillation.
334
MOA of Rivaroxaban/Xarelto
direct inhibiton of factor Xa
335
Char of Rivaroxaban/Xarelto
PO only
336
side effects of Rivaroxaban/Xarelto
Bleeding. Clinical trial data have shown that Xarelto allows for predictable anticoagulation with no need for dose adjustments and routine coagulation monitoring. However, these trials have excluded patients with liver disease and end-stage liver disease; therefore, the safety of Rivaroxaban in these populations is unknown.
337
class of streptokinase
Thrombolytic (clot buster)
338
indication of streptokinase
acute myocardial infarction, acute ischemic (non-hemorrhagic) stroke, acute D.V.T. or P.E.
339
MOA of streptokinase
Activates plasminogen to plasmin. Plasmin digests fibrin and fibrinogen forming degradation products.
340
Char. of streptokinase
Isolated from Streptococcus species - group C beta-hemolytic strep. I.V. administration only, half life ~1 hour....Strict inclusion and exclusion criteria must be met before Streptokinase or any of the thrombolytic agents can be used.
Exclusionary criteria include the amount of time passed since M.I. or stroke and such conditions as active internal bleeding, a history of intracranial hemorrhage, a intracranial neoplasm and head trauma within the previous 30 days. (Additional exclusion criteria exist.)
341
Side effects of streptokinase
Bleeding. Enhances risk of bleeding caused by aspirin, NSAIDs heparin, Coumadin and the anti-platelet agents.
342
Antidote to bleeding in the class of drugs known as "clot busters" (streptokinase)
Aminocaproic acid (Amicar) is a plasmin in-activator and antifibrinolytic. It is utilized for bleeding that occurs as a result of streptokinase and other agents in this class of drugs referred to as the “clot busters”.
